↑ Return to Journalism

WSUV Neuroscience Student Journalism

 Making pregnancy safer for baby and mother: What you feel during pregnancy can also affect your baby

By Elsa Gomez, 2018 WSU Vancouver Neuroscience Student



Imagine you’re expecting the arrival of a new child and all the emotions that come with it. The positive: excitement, happiness, joy, and the not so positive ones like anxiety or stress.  Now imagine if your baby could also experience these emotions with you, yes, even the bad ones. Anxiety, sadness, and stress, for example, are all common symptoms occurring in women experiencing postpartum depression. The recommendation for mothers to be screened for depression, both during pregnancy and after birth, is important, as evidence shows 1in 7 women experience a postpartum episode within a year of giving birth.

Many expecting women are reluctant to share their symptoms with their doctors and care-givers, and are often left to navigate their already stressful journeys on their own. This in turn leaves many mothers undiagnosed.

Mayra Douglas, 30, of Juneau, AK., wasn’t screened for depression during her first pregnancy or after delivering. “After you leave the hospital you are left to make your own appointments and having a new baby posses a lot of its own stressors,” she said. Ms. Douglas became part of a community of new mothers who barely sleep, experience overwhelming anxiety, and depressed moods.

A recent government appointed panel has raised the issue for mothers to be screened due to increasing evidence on the prevalence of maternal depression. Current research shows that postpartum depression is being experienced not only by the mother, but by their babies too.

Researchers at the University of Oregon have recently examined whether increasing maternal depressive symptoms affected infant stress and later cell health. Researchers used procedures designed to observe how infants respond to stressful situations created by changes in maternal care, and found that infants exposed to maternal depression experience stress responses that lead to cellular damage.

How does a mother’s depression affect their babies cells? Inside every person exists a cellular cookbook within your DNA. This cookbook is comprised of 46 recipes, formally known as chromosomes, 23 from your mother and 23 from your father, each respectively paired together. The 23 pairs are protected with caps known as telomeres, and these caps are what researchers are now focusing their attention to.

The length of telomeres is affected in all of us by genetics and age. Their length has been used as a biological indicator of age and health, because their shortening is responsible for a range of health issues including aging and cancer. Telomeres can degrade more quickly when a person suffers from psychological stress and in the case of infants, stress brought on due to exposure to their mother’s depression.

Benjamin W. Nelson, a Doctoral Student at University of Oregon, found that the increased levels of stress hormones released in babies exposed to maternal depression was responsible for their shorter and fewer protective telomeres. Nelson measured the level of the stress hormone known as cortisol, and telomere length in infants by collecting saliva samples. Nelson was able to show that infants with higher cortisol stress responses were more likely to have shorter telomeres at 18 months of age. His research shows that maternal depression can impact mothers and their babies.

What you feel during and after pregnancy can have an effect on your baby’s health. Providing awareness and educating communities about maternal mental illness may reduce in the reluctancy of expecting mothers to share their symptoms and feeling during pregnancy. Supporting mothers in their mental health journey most continue to be a priority as it affects them and the health of their new baby.

   Sleep: How Important Is It?

By Jannea Mantz, 2018 WSU Vancouver Neuroscience Student

Have you ever been so tired that you couldn’t form words, or forgot where you were going? Like when you get in your car after a long day’s work and all of a sudden, you’re parked in your driveway and you can’t remember how you got there. A lack of sleep can interfere with your daily function. Sleep is important for overall health and wellness. Sleep can improve your mood, heart, and strengthen memories learned earlier in the day. Sleep also increases lifespan, lowers stress, and diminishes inflammation. It helps to restore the body in many ways, by conserving energy, regulating the body’s internal temperature, and helps in tissue recovery.



30% of American adults get less than 6 hours of sleep a night. A lack of sleep is harmful for not only the body, but the mind as well. Think of it like tooth decay, if you don’t take care of your teeth, eventually they’ll rot away. Lack of sleep leads to cognitive dysfunction. Someone who has chronic sleep deprivation, which can come from long work hours or study hours, has compromised nightly sleep on a regular basis. This situation is very common nowadays and is something many of us can relate to. I know I’m guilty.

People like me, who have experienced this type of sleep loss need to be aware of the effects it can have, which range from fatigue, daytime sleepiness, weight gain or loss, clumsiness, depressed mood, reduced sex drive, and most importantly trouble with certain brain functions, such as reasoning, language, attention, and memory deficits. These effects can disrupt a person’s quality of life.

Being able to cope with sleep deprivation can depend on several factors, especially age and gender. Recent studies performed by sleep scientists at Uppsala University show that, in comparison to men, women have impairment of their working memory, which is part of the short-term memory involved in tasks, attention, and learning. Sleep deprivation is associated with these impairments. These studies show that women who experience lack of sleep have difficulty performing tasks involving memorization and learning. Imagine that you’re at work and the company is implementing a new protocol, yet you stayed up all night because of some event you attended and you are having trouble focusing. Your boss walks in and says that this protocol will be up and running by the end of lunch. You are so tired that you can’t understand the details of this new protocol. Oh no! What are you going to do now? These women who experience these impairments are also unaware of their diminished performance, suggesting women are at risk of overestimating their performance while sleep deprived and are at risk of causing mistakes. This lack of awareness of their impaired performance can be a problem in many occupations.

It can lead to increased risk of accidents and misjudgments due to the lack of speed and accuracy that are involved in sleep deprivation. Individuals who work in the evenings, like warehouse workers, those that work in transportation, and health care employees are among those that are at high risk for sleep deprivation and therefore more likely to cause accidents. Recently, a Metro-North engineer in New York derailed a train while going 82 mph around a corner after he had nodded off. He killed four passengers. Chernobyl, one of the world’s worst nuclear disasters caused numerous deaths and a huge amount of fallout. The engineers working on that day had been working for over 13 hours, late into the night. Their judgement may have been compromised, creating a, possibly, avoidable disaster. Gregory Cousins, the third mate of the supertanker involved in the Exxon Valdez oil spill was allegedly asleep at the wheel when the crash took place, spilling 258,000 barrels of crude oil. These are just a few of the many accidents that have occurred due to sleep deprivation.

These findings mean that a fair amount of attention should be given to women that have to deal with and perform under these conditions. Giving more attention to these women by providing extra time off, the possibility to work from home, or creating shorter shifts, can possibly prevent any set backs or mishaps that may occur due to sleep deprivation.

So next time you ladies out there are thinking about pulling an all-nighter, whether it’s to get that project at work completed or to study for that important exam, you may want to think twice. Getting some well needed rest will actually help you perform better and be more precise when you do. If you know an individual who experiences lack of sleep on a regular basis try to pay more attention to how they are functioning and whether or not it may be an issue. Most of all, try to get some sleep.

 Brain-gut correspondence: Could your intestinal integrity be contributing to drastic changes in your brain?

By Bradley Mahoney, 2018 WSU Vancouver Neuroscience Student



Is it possible that  an individual’s intestines  could be  causing  the development of different neurodevelopmental conditions such as autism? This is certainly a more reasonable explanation for the development of autism when compared to the case proposed by the anti-vaccinating mothers of Ashland, Oregon. In case you are unware, the mothers of Ashland, Oregon have the lowest rates of vaccination in the entirety of the United States! In addition, this community has been at the forefront of the anti-vaccination “war”. Autism is under the umbrella of autism spectrum disorders or ASDs, which are conditions characterized by progressive, and widespread alterations in an individual’s ability to communicate and interact socially. These disorders are extremely prevalent  in the US, as well as other developed countries such as Japan. Approximately 1 out of 150 children born in the US  are diagnosed with ASDs.

Now you may be asking, how could intestinal health have anything to do with the development of autism? While the direct connection is still yet to be discovered, something called intestinal permeability (IPT) could be contributing substantially. Intestinal permeability is essentially the ability of substances in your small and large intestine to cross the lining of the gut, and enter the blood. While intestinal permeability itself is not directly causative of autism, it is the dysfunction of the child’s intestinal barrier and an increase in IPT that has been linked to the development of autism. Furthermore, this increase in IPT has been shown to cause many other systemic changes within the body, including intestinal swelling or inflammation, and increased fat build up.

How is an increase in intestinal permeability caused? To answer this, we must look at the microbiota of the gut of a child with autism, and the integrity of their intestinal barrier. In a broad scope, the microbiota of someone’s gut is the trillions of microscopic friends living just above their waist. These little “critters” help us in a variety of ways, from helping us break down the food we consume, to helping regulate our immune systems, or our natural response against harmful bacteria. However, not all of the bacteria in our microbiota are beneficial, in fact, many will seek to harm us if given the proper opportunity. These opportunities can be frequent if there is a disruption of the integrity of the individual’s intestinal barrier.

A person’s intestinal barrier helps keep out harmful substances, and bacteria, through a tightly intertwined community of “gut” cells. These “gut” cells are held together by structures known as tight junctions, which only allow certain particles to cross into the bloodstream. As shown in the graphic at the start of this article, when these junctions become damaged, harmful substances, toxins, and undigested food particles enter the bloodstream. When these sneaky particles enter circulation, they are able to influence the individual’s behavior through something known as the gut-brain axis. Recent research has demonstrated that disruptions in an individual’s microbiota, and hence there IPT, can severely impact development of emotional behavior. This profound impact was observed in rat models, and was also shown to be significantly affected by antibiotic administration. The connection between the gut and brain allows chemicals of the digestive tract to influence the brain. In summation, increased intestinal permeability via microbiota disruption has been strongly associated with the development of many neurodevelopmental and autoimmune diseases such as type I Diabetes

Now where to go from here? This research highlights an interesting trend that may often be overlooked when treating and diagnosing those with autism and similar conditions. Specifically, the observed trend of intestinal barrier dysfunction in those diagnosed with ASDs Interestingly enough, research done in just the last year has shown that stimulation of a nerve known as the vagus nerve may prove to be a powerful tool for the treatment of ASDs. Stimulation of this nerve has been shown to decrease the communication deficits seen in children with ASDs and other similar disorders when coupled with behavioral therapy. This decrease in communication deficits is thought to be due to a decrease in IPT and a restoration of the child’s intestinal barrier. Overall, recent research on the topic has shown many novel diagnostic and potential treatments for ASDs, and these options may be the saving grace for families with children who suffer from severe autism. [1]

[1] If you’re interested in reading further into this cutting edge research yourself, you can do so here!

Are Magic Mushrooms Really “Magic” for Severe Depression?

 By Richik Neogi, 2018 WSU Vancouver Neuroscience Student

Living with major depressive disorder (MDD, often referred to as clinical depression) is like slowly being pulled under water. You can hear everyone enjoying the beautiful day above you, laughing, having conversations, and just marveling at the beauty of the outdoors, but you cannot experience this because you are drowning and it is cold, dark, and lonely. At first you might struggle to fight the undertow, but eventually you get tired and wait for death to consume you. Yet, to your horror, you cannot die. I find that this analogy accurately describes many of the symptoms of my MDD, but each depressed individual has his or her own way of describing depression. Over 16 million Americans have had a major depressive episode, out of which approximately 10 million reported significant functional impairment as of 2016.

The largest systematic analysis of effective pharmacological treatments for depression in the United States (the STAR*D trials) found that a startlingly large percentage of individuals – up to about a third – did not report remission (full recovery from depression) upon first-line and second-line treatment with two different medications or cognitive-behavioral therapy. Most of the pharmacological tools for treating depression available to psychiatrists are blunt tools that affect a widely-spanning system of nerve cells the release the chemical serotonin. They must be taken daily and do not produce full remission in many patients. Perhaps the most well-known antidepressant drug is Prozac, a SSRI (selective serotonin reuptake inhibitor). SSRIs/SNRIs come with sometimes intolerable side effects and discontinuing many of them can cause extremely unpleasant side effects, even after the last dose has been consumed (withdrawal). Antidepressants may take weeks or even months to reach full efficacy, which poses an unacceptable risk to a population in which suicide rates are high. The hunt for a rapid-acting antidepressant for patients with severe, treatment-resistant depression has been on for decades now.

When you think of psychedelic drugs, what do you think of? Even in a sample of university students, most were reluctant to acknowledge their medicinal benefits, and many associated hallucinogen use with poor mental health. You can imagine what public perception of psychedelic drugs in the general, more conservative population is like. This, combined with the fact that most psychedelic drugs are Schedule 1 controlled substances (in the same DEA schedule as heroin and PCP) makes it extremely difficult for scientists to study their potential uses as medicines. Although there is a large body of research on psychedelic drugs dating back to between the 1950’s and the year 1970, many of these studies were not conducted in a manner appropriate for scientific research today (i.e. they lacked controls, used unethical clinical protocol, or had a poor study construction in general). Since the 2000’s when Charles Grob introduced the idea of using psilocybin to treating obsessive-compulsive disorder and other groups have since confirmed beneficial effects of psilocybin in treating obsessive-compulsive disorder (OCD). We know a lot about how classical psychedelic drugs affect functioning at the neuronal, circuit level, and behavioral level, but we know little about how these drugs impact large networks of neurons.

Imagine the brain as a jar of beads (“networks”), each containing several smaller beads, connected by several different threads. All of these smaller beads are connected, but not all of these larger beads are. The inner beads (“nodes”) are connected by a multitude of smaller, but more malleable threads, some of which remain within the larger bead and some of which exit the larger bead and join various outer threads. One bead, both inner and outer, “talks” to another by oscillating against it. These outer beads represent individual networks in the brain. The difference in the subjective state that the individual in whom the brain is contained is a result of this differential wiring. These differences in intranetwork wiring have been observed in depressed patients. The bottom line is that depression isn’t as simple as a chemical imbalance; there are complex, network-based changes in the brain responsible for the symptoms someone is experiencing. It’s not something that can be quickly reversed by any drug on the market today because currently available drugs target the differences in wiring indirectly. However, there are many illicit drugs such as the anesthetic ketamine and psychedelic drugs like psilocybin that can disrupt connectivity within networks. Can these drugs potentially be used to treat depression?

Robin Carhart-Harris, a researcher at the Imperial College London, was among the first researchers to image the healthy brain on psilocybin (which is converted to psilocin almost as soon as it enters the body), the active component in “magic mushrooms.”  Importantly, he and his colleagues found that intravenous psilocybin decreased blood oxygenation in key hub regions, most of which were located in the default mode network, a key orchestrator of the resting mind (i.e. responsible for rumination). Direct electrical desynchronization of these hub networks within the brain during the psilocybin-induced psychedelic state was later demonstrated using magnetoencelography, a method of recording electrical activity of neurons (in particular their firing frequency and amplitude). Importantly, this desynchronization was observed to be the greatest in integrative regions of the brain that receive input from a variety of networks.

Depressed patients are locked in a maladaptive rigid form of thinking. Psychedelic drugs temporarily alter the number of different possible connections our beads can make in our “beads-within-beads-on-strings” analogy. One can see how this enhanced flexibility of nodes can both be both extremely beneficial to treatment-resistant depressed patients and potentially dangerous. One mitigating factor here is that the effects of psychedelic drugs and psilocybin in particular seem to be restricted to a few key areas, likely as a result of the increased density of the receptors that psychedelic drugs bind to.  Carhart-Harris and colleagues therefore took a cautious approach to administering psychedelic drugs to humans. Up until recently, most of the imaging in healthy subjects receiving psilocybin measured acute effects. Carhart-Harris’s group optimized the protocol for administering psilocybin safely to healthy people in initial studies and then repeated this protocol twice spaced two weeks apart, first at a lower dose to gauge negative reactions. Those that experienced significant anxiety during the trip experienced more positive outcomes, though the duration of this anxiety was positively correlated with the lack of response to treatment. It is important to emphasize that under these conditions, none of the participants reported increased symptoms of depression. In fact, in a significant proportion (18 out of 19) reported improvement in mood the five weeks after treatment and none showed worsening of depression in the 5 weeks after the second dose. More importantly, 47% of the participants reported clinically significant reduction in depression-related symptoms after several months. Reduction in symptoms were correlated directly with changes in intranetwork connectivity.

 What is chronic pain doing to your brain?

By Dane Collier, 2018 WSU Vancouver Neuroscience Student

Imagine all the people you know who might be suffering from a chronic pain condition. Chances are you know several, whether they told you about it or not. People with chronic pain conditions like irritable bowel syndrome, migraines, lower back pain and phantom limb pain tend to learn to live with the pain as it persists for greater than six months. WebMD recently published a guide to living with chronic pain to provide some relief for those scouring the internet for solutions.

Chances are probably either feel chronic pain yourself, or feel bad for these people because of the pain that they experience. An article published in the journal Pain would suggest that we have greater reason to be concerned about those in chronic pain. The different compartments of the brain of chronic pain sufferers are changing their interconnectivity as a result of constant pain. This means that the different parts of the brain are talking to one another differently with chronic pain.

The brain is divided into several unique areas that each have their own job. Even the most mundane processes of the brain, like writing your name or recalling a phone number, typically incorporate a variety of these areas to work together. Consequently, anticipating and experiencing pain requires using multiple brain regions. These unique areas work together to paint the whole picture of the pain that is being experienced.

There are networks of neurons in the brain that allow these different regions of the brain to communicate. Chronic pain sufferers have characteristic interconnectivity of their brain as a result. This interconnectivity in brain regions such as the insula and cingulate cortex, which participate in the emotions and learning of pain, is the result of frequent stimulation of those brain regions. Repeated stimulation from chronic pain strengthens networks of the brain as we form associations and as the brain tries to anticipate which areas of the brain should be firing together. This was discovered in humans by comparing magnetic fields produced in the brain as a result of pain in chronic pain sufferers and controls.

Chronic pain influences the representation of our body parts in the brain. Depending on the intensity and location of pain experienced, the representation of that painful body part can be decreased or increased. The magnitude of change in representation in the brain is directly related to the intensity of the pain experienced. Greater pain leads to greater reorganization of the brain. In the brain of a chronic lower back pain sufferer the representation of the back is increased. This means that more brain real estate is devoted to the back making it disproportionate to other body parts. This prioritizes the back despite its actual size remaining the same.

The brain is able to change in these ways due to a characteristic of the brain known as plasticity. The plastic nature of the brain allows for these changes to take place as a result of chronic pain. However, plasticity is also the reason that there is hope for chronic pain sufferers. While the brain can change from frequent input, those changes may revert when input returns to normal levels. This means that when chronic pain stops, the interconnectivity of the brain and its representation of the body can return to normal.

This should highlight the necessity for effective and affordable pain treatments to prevent and reverse these changes to the brain. In the meantime the American Society of Regional Anesthesia and Pain Medicine as well as the American Chronic Pain Association strive to inform chronic pain sufferers of the treatments available to them and make them as accessible as possible.

 Living in a Dark Room

By Saray Farias-Pulido, 2018 WSU Vancouver Neuroscience Student

Imagine you’re trapped in a dark room. You hear people laughing on the other side of the door and you want to join them but no matter how hard you try, you can’t get out. It’s just you, alone, in a dark cold room. Imagine your biggest fear is living in this dark, cold room. This is what life feels like to people living with Major Depressive Disorder. Depression is the leading cause of disability in the world and its prevalence continues to rise. Suicide, caused by severe depression, is currently the second leading cause of death for people between 15-29 years old.



So, what exactly does depression look like? It would be difficult to point out someone on the street suffering from depression. Depression is a mood disorder that can affect anyone. It’s possible that someone you know has experienced a depressive episode without you knowing it. Some common symptoms of depression include persistent sadness or “empty” mood, loss of interest in things you used to enjoy, feelings of guilt or worthlessness, and irritability. In order to be diagnosed with depression, these symptoms need to persist for more than two weeks.

Now the question is, what causes depression? The answer to this question is both very complex and not very well understood. Depression is a neurological disorder that we do not know much about. For a while depression was thought to be caused by a chemical imbalance in the brain. This chemical imbalance was the result of there not being enough “feel good” chemicals in our brain, such as serotonin. This chemical is what’s responsible for that warm feeling you get when you eat chocolate or get a big hug.

To combat depression, antidepressants were created in order to correct this chemical imbalance. Common antidepressants work by preventing certain proteins from picking up serotonin and recycling it. By preventing the recycling of serotonin, the brain can use the available serotonin for longer than it usually would. This gives serotonin more time to contact the surrounding nerve cells, telling them that we feel good. These antidepressants have helped many people but currently they are only effective for about 33% of the people who use it. Another problem with antidepressants is that they can take over two weeks to be effective.

Now research is focusing on the lack of new nerve cells, and how they can contribute to depression. Dr. Douglas Bremner and colleguesnoticed that people suffering from depression tended to have a smaller hippocampus, a brain region that regulates emotions and memory, than those who did not. Depressed individuals had a 19% smaller left hippocampus even after taking into account other factors such as education and age. They discovered this by comparing MRI images of the brain between patients with a history of depression and healthy subjects. Less growth in these brain regions  means that nerve cells may have a harder time communicating with each other. Scientists have speculated that the reason common antidepressants take so long to have an effect is because the brain needs to be kickstarted into creating new cells. This discovery resulted in a renewed attempt in the development of additional treatments for depression. These new treatments are focused on encouraging cell growth in the hippocampus and other regions affected by depression.

There is still a lot to be learned about the causes of depression before fast and effective treatments can be developed. Current treatments have helped many people suffering from depression and with more research, new treatments can be developed to help even more people. With so many people affected with depression, it’s important we find a way to unlock the door to that dark, cold room.

 Losing Weight with Your Brain

By Anthony Ziegenfuss, 2018 WSU Vancouver Neuroscience Student

Everyone wants an easy cure to obesity. Ads full of one magic pill, or body wrap, or tricks that doctors hate, all claiming to make the pounds fall off. And none of them work.

Obesity or even just being overweight is a problem for 70% of Americans over 20. This means that most of America’s adults are overweight. The consequences of being overweight or obese are more than having a hard time fitting into a chair or climbing the stairs. It gets worse. Being overweight can lead to heart disease or diabetes among other problems. Heart disease alone claimed the lives of 633,842 Americans in 2015.

As of right now the primary solution to being overweight or obese is to eat better, eat less, and exercise. If the weight problem progresses to the point of being morbidly obese there is a surgery that helps called gastric bypass. The surgery involves changing the way the stomach and small intestine connect and making the stomach two connected pockets instead of one larger one. This option can save the lives of people that progress to the point of morbid obesity but is not available to those who are not morbidly obese and carries the risk of any surgery regarding infections and complications.

One of the largest hurdles for people trying to lose weight is maintaining the willpower to reduce the amount of food they eat. Researchers with the National Institutes of Health have come up with a possibly revolutionary way of helping to fight the urge to eat unhealthy food. They applied an electric shock to an area of the brain that is involved in decision making, the dorsal prefrontal cortex, and allowed participants to eat candy and other snacks. The therapy lasted for 40 minutes each session. The participants reported the taste of the food and how much they ate. The researchers reviewed the results after three inpatient sessions and found that nothing seemed to be happening.

Despite the troubling lack of results of this method the researchers pressed on with the study and began outpatient treatments for 4 weeks with 3 sessions per week. They found that after 15 total sessions of this electric stimulation there was a noticeable difference in the participants. The participants reported to be less hungry and to find the unhealthy food less appealing. These miraculous effects don’t come without a downside however. The participants reported: headache, neck pain, scalp pain, scalp burn, tingling, skin redness, sleepiness, trouble concentrating, and mood changes. Except for skin redness, this laundry list of illnesses may be chalked up to the apparatus used to apply the electric shock, as the control groups had similar complaints to the experimental groups. The duration of the good and bad effects of the sessions were not thoroughly investigated and leaves room for future research into this method of weight management. This shows a critical change in the way the participants think about the food.

The food itself seemed to be less desirable and this change opens the door to the possibility of using this treatment to help reinforce a person’s willpower. If there is no urge to eat extra and unhealthy food, it may not be as difficult for someone to eat less and lose weight, and all it takes is 15 sessions of electric stimulation.

Disease-Free Water Bottles

 By Anthony Almonte, 2018 WSU Vancouver Neuroscience Student

Stop right there! That plastic water bottle you are drinking from is probably giving you cancer making you sick! It has been confirmed that the chemicals that make up a plastic water bottle leech into your water and when consumed this can result in dangerous side effects. These chemicals are linked to diabetes, obesity, heart problems, infertility, and many types of cancers. These harmful chemicals are mostly found in products containing plastic. When you think about it, plastic is found everywhere. It’s found in the lining of your canned foods, cleaning products, deodorants, shampoos, conditioners, cell phones, and your mom’s make-up is held within plastic containers.

The chemicals that reside within these plastic containers are known as endocrine disrupting chemicals, or EDCs for short. EDCs do what they are named for: they are chemicals that enter the body and disrupt the endocrine system. The endocrine system is responsible for regulating many of our bodily functions by balancing hormones. When the body needs to regulate a bodily function, a region in the brain receives messages to release hormones. Hormones play a huge role in hunger, thirst, regulating body temperature, mood, and sexual desire.

Let’s think of a lock and a key, where a specific key (the hormone) will open a lock (a receptor). These receptors are padlock-shaped proteins which are found all throughout our cells. They receive signals that then get passed on to other cells leading to a reaction. When the wrong kind of key tries to open these locks, it gets stuck in place, blocking the correct key from doing its job. EDCs are known to mimic the shape and function of hormones in the body.

Many dysfunctional disorders result when hormones aren’t allowed to do their jobs. Hormones are necessary for growth, especially in the early stages of development. Links have been made to There have been many cases in which deformities in children and exposure to EDCs. due to these unfortunate processes. We’ve heard of the phrase “teenagers and their raging hormones!”, well there are direr consequences to the imbalance of these hormones. Studies have related EDCs and shown that kids are going through puberty at earlier ages every year conflicting with their natural sexual maturity.

Good news! Treatments to balance theses hormones exist, such as hormone therapy and medical prescriptions. The bad news is that treatments can induce many side effects like fatigue, weight gain, memory loss, and much more. It may be difficult, but these toxic chemicals can be avoided. To avoid these endocrine disrupting chemicals, one can should become more aware of the foods and drinks that one consumes.

I’m sure you have probably been told not to leave your water bottle in the car. This is because the sun will heat up those chemicals where they will seep into your water and when consumed, they’ll accumulate in your body over time. Although the bottle might say BPA-free, BPA is only one type of an endocrine disruptor. There are still many more chemicals contained within these plastic containers. Of course, more research is needed in this field of study to prohibit these endocrine disrupting chemicals from entering the market. Hopefully one day with the power of research, more attention on the profound effects that these chemicals have will alert the world to strive for all plastic containing products to be manufactured as EDC-free.

 Are we the guinea pigs of cell phone radiation?

 By Holly D’Andrea, 2018 WSU Vancouver Neuroscience Student

In 2017 it was estimated that approximately 95% of American adults own a cell phone. It has been considered the most widely adopted consumer technology ever, so much so that some even joke that it has become an extension of the human body. Aside from making phone calls, we now use our phones to make our next purchases, take photos, find our next date, surf the web and even find the nearest stranger to give us a ride to our next destination. But it doesn’t stop there. In 2017 it was reported that consumers are averaging  2 hours and 51 minutes of cell phone time per day for adults, and over 4 hours per day for people under the age of 18.

Does all the convenience of a cell phone come with unwelcomed health consequences?  In order for cell phones to work, they must emit signals via radio waves. These waves are a form of electromagnetic radiation (EMR). EMR can be thought of as invisible waves traveling through the air that communicate between our phones and neighboring cell phone towers. It is essentially the signal to our phone and it allows cell phones to communicate back and forth. EMR is absorbed by the human body and is classified based on the amount of energy it carries; ionizing radiation is considered high frequency while non-ionizing radiation is considered low frequency. Cell phones are non-ionizing and share the same frequency of EMR as microwave ovens. But, we’re not holding microwaves to our heads for hours a day, carrying them in our pockets and we’re likely not sleeping next to them at night. Cell phone manufacturers have also acknowledged the concern of EMR and have issued fine printed safety warnings in your user manuals that you likely have never seen. Want to know what your iPhone has to say about EMR? Pick it up and click on Settings > About > Legal > RF exposure.

So what effect does EMR from cell phones have on the human body? Scientists are hard at work trying to answer this question. Studies have clearly found associations between the duration of cell phone exposure in males to reduced sperm motility and viability. However, how cell phone EMR is affecting the developing brain and if it is causing brain tumor growth is currently up for debate. While studies have shown links between the amount a time a person uses a cell phone to an increase risk for brain tumor growth, others have failed to find that link.

In a 2015 study, researchers discovered that when a person began using a cell phone before the age of 20, their risk for developing a glioma brain tumor increased by 20%, when compared to first time users after age 20. Interestingly, these glioma tumors were more prevalent in regions of the brain that we hold our phones closest to. Researchers believe the reason cell phones may do more damage to earlier users is due to the vulnerability of the developing brain, and a thinner skull bone. Furthermore, after a review of the current research in 2011, the World Health Organization deemed it necessary to classify cell phone EMR as a possible human carcinogenic. However, their website claims that based on research to date, cell phones do not cause adverse harm to human health. They also state that researchers have failed to find a link between cell phone EMR and brain cancer in animals.

The research is debatable and experts agree this is due to the short amount of time cell phones have been in the population, the ever changing ways they are being used, and the slow growth of brain tumors. But, whether we like it or not, we are all guinea pigs of EMR and more time is needed before researchers can reliably deem it safe for human health.

Does your food irritate you?

 By Jeremy Dunford, 2018 WSU Vancouver Neuroscience Student

“You should eat your meals on the toilet.” or “Can’t your doctor do something about your stomach pain?” are some statements I have heard when people discuss their inflammatory bowel disease (IBD) with friends and family.

Over 3 million Americans suffer from IBD. These statistics include those who have been diagnosed and don’t include children or those who suffer undiagnosed. This is a staggering amount that is on the rise. The breadth of symptoms is large and goes to extremes. From diarrhea to constipation, anxiety to depression, and cramps to strict diets, the list goes on and on.



People with IBD experience discomfort and quality of life changes. The symptoms vary from person to person and there is no cookie cutter response to the condition. What if you were late to work because of an extra trip to the bathroom? How about being constipated for a week followed by a week of diarrhea? Out to a concert and have to fight your body while waiting in line for bathroom? Ever consider the depression or anxiety associated with managing the disease, which could then cause a flare up? The scenarios are endless and the solutions are limited. Many groups have come together to support each other through humour and empathy.

While humour and empathy are helpful, they are far from a cure. The causes for IBD are unknown and is broken into two main forms called ulcerative colitis and Crohn’s disease. Current treatments extend just as wide as the spectrum of symptoms. Those with severe aspects of the disease are often issued steroids, immunosuppressants and/or could require surgery. These all have risks and the goal is just to reduce the symptomatic expression in hopes for a remission. Less severe cases utilize a change in diet, reduce stress, and getting more rest to feel better.

Through technological advances and a deeper understanding of our biology, we are better able to define disease states. With chronic autoimmune diseases more prevalent in today’s society, it is important that we better understand them. This can be done by educating ourselves through good research sources, honestly conveying our experiences to health care professionals, and applying the education to practice in our lives. In doing so we can all experience better quality of life, by treating and being treated, in the most effective ways possible.

 Autism: Not just for boys

By Mary Ruth Marigomen, 2018 WSU Vancouver Neuroscience Student

Sugar, spice, and everything nice; snips and tails and puppy dog tails. Girls and boys have always been viewed differently. Society has created this great divide between the two genders that extend well into adulthood: women are from Venus, men are from Mars. So, if females and males are so different from each other, why are we diagnosing Autism Spectrum Disorder (ASD) across genders based only on studies done on boys?

Imagine yourself at the park, enjoying a nice Saturday afternoon. As the day wears on, you find yourself taking notice of three little kids of roughly about the same age. The first kid, a boy, appears to be staring at a single page of a book—no pictures, just a barrage of words—for hours, not minding the chaos in the background. The second kid is another boy who has been grabbing everyone’s attention because of his crying every time another kid touches him; he seems to put so much effort into finding himself a space away from the other kids. Finally, another child you have been observing is a little girl who has her doll all tidied up, its hair all nice and combed religiously. The behaviors of the two boys may stand out to you and make you suspect that something is amiss with them. But how about the little girl? Is it really that uncommon for little girls to groom their dolls? You probably see that behavior in your daughter, your sisters—or if you are a woman who had a doll at some point—in your younger self. What if I tell you that putting you at the park was my way of putting you in my shoes; that putting you in a place of observing these kiddos was in turn, putting you in my position as a behavioral therapist? What if I tell you that all three children above are not just normal kids, but patients with autism? Yes, even the little girl.

It is widely known that autism is more common in boys than it is in girls. However, researchers are rethinking their stance on these thoughts—and rightly so. Why? Because it turns out that autistic girls often get misdiagnosed or have a delayed diagnosis.

Autism has many faces. Up until now, we are familiar with only a handful of them: repetitive behaviors, known as “stereotypy” in the trade, which include fixation on numbers, letters, and shapes; and social inadequacies: it’s easy to wrap our heads around an autistic child avoiding touch or eye contact for dear life. But what if these hallmark symptoms, our go-to reference before we could diagnose a child with the A-word, are not as common in the other half of the population of autistic people? As it turns out, repetitive behaviors look different in girls. While in boys they are pronounced as obsession with letters, numbers, or shapes, in girls, they may appear inconspicuous—like keeping one’s doll nicely groomed, or listening to the same Disney song over and over again. Furthermore, girls with autism tend to be more social than boys. One study evaluated the developmental levels of boys and girls with autism compared to those of normal-developing children. They found that autistic girls were behind normal girls in levels of development but were on the same levels as normal-developing boys. Research shows that not only are the brains of autistic girls different from those of normal-developing girls, their brains are also different from those of boys with autism. These biological differences, in turn, translate into behavioral differences—behavioral differences that are infrequently explored in ASD research. No wonder such a diagnosis in girls is so elusive.

After this waterfall of information about how our methods of diagnosing autism is faulty, we need to ask two vital questions: why do we care and what is our next step? We care because misdiagnosis in autistic girls pulls them further away from being treated; they can go on to develop other illnesses such as depression and anxiety due to these unaddressed issues. Furthermore, early detection of autism is crucial for effective treatment outcomes. All the time and other resources wasted on addressing wrong diagnoses or the lack of answers, count towards the recovery of an autistic girl who is already taking on an unthinkable challenge in life. How are we to move forward from this? We must revamp our methods for diagnosing autism. Myriads of observational studies need to be done to zero in on what makes autism different across genders. These observational studies need to start in places where these children spend a great deal of their time: at home, at school, at parks.

So, imagine yourself at the park. But this time not as a behavioral therapist, but as a parent, a babysitter, or an observer who’s casually enjoying the day. Look at the behaviors that children—specifically, little girls—are exhibiting. Autism has many different faces. Don’t just look; observe. Pay attention. For if you look closely enough, or long enough, you might just see autism showing its less obvious face. And recognizing such a face could change a girl’s life.

 Like Lazarus: Consciousness Restored by Vagal Nerve Stimulation

 By Travis Nash, 2018 WSU Vancouver Neuroscience Student

New hope for severely debilitated patients- A promising new experiment demonstrates that patient consciousness is restored by vagal nerve stimulation.

Imagine getting into a car accident as a teenager and regaining consciousness when you are in your early thirties. This would be a frightening and confusing experience, to say the least, but it certainly beats the alternative of remaining unconscious until meeting the end. In a recent study conducted by a research team out of France, a man who had been in a coma-like state for 15 years, suddenly regained consciousness after researchers and neurosurgeons stimulated one his major brain nerves  for 6 weeks.

Specifically, the patient suffered from a medical condition called “persistent vegetative state.” A persistent vegetative state (PVS) is a serious medical condition similar to a coma. The true number of patients who suffer from this condition is not known, but it is estimated to be somewhere between 40 – 168 people per million in the United States alone. People can sustain this disorder from a number of causes such as a head injury, accidental toxin ingestion (typically depressant such as tranquilizers), or even from certain degenerative diseases such as encephalomyelitis. Before this trial, there were no treatments for this condition. If you were to fall in your home and slip into a PVS, then you would receive basic medical care such as nutrient management and disease prevention. After that, doctors and family would simply wait and hope for a recovery.

The scientists in this experiment were inspired by previous work that found awareness in humans could be increased by stimulating a certain network that connects several brain regions together, collectively referred to as the thalamic-cortical axis. The problem with this technique was that it required making holes in the skull and stabbing fine-stimulators into the brain. This is invasive and not practical for a general treatment.

Vagal nerve stimulation is accomplished by wrapping a stimulator around the vagal nerve at the level of the neck. goo.gl/dXRVFp

Vagal nerve stimulation is accomplished by wrapping a stimulator around the vagal nerve at the level of the neck. goo.gl/dXRVFp

Through the creativity and insight of these scientists, however, they were able to see that this same pathway could be stimulated through a less-invasive route. There is a major nerve called the vagus nerve which exits the skull and travels into the chest, to the primary muscle used for breathing. This nerve can both send and receive stimulation.

Armed with this knowledge, the scientists had a team of neurosurgeons wrap a small-metal wire around the vagus nerve at the level of the neck, connect it to a stimulator, and place the stimulator under the skin of the chest in a fashion somewhat likened unto a pacemaker (see picture). After applying small controlled shocks to the nerve for 6 weeks, the patient eventually started to show signs of improvement.

For the first time in 15 years, the patient was able to express emotions by smiling at the voice of his parents and crying to the sound of familiar music. At the end of the experiment, he was even turning his head in the direction of a family member or doctor as they said his name.

Although the patient is still unable to speak or get out of bed at this time, his response and progress is unlike anything we have seen so far. This study is a promising new avenue for even more understanding of how this condition works and how we could someday permanently treat it. This finding might even extend to help us discover a revival for people in comas in the future by similar activation of the awareness centers in the brain.

 Old Viruses and New Ways of Thinking About Memory

By Jereme Wingert, 2018 WSU Vancouver Neuroscience Student

Most people probably have a long history with viruses. We have all probably called into work sick countless times with the common cold which is caused by viral infections. It is also not uncommon to hear about more severe viral infections in the news such as bird flu, swine flu, or Ebola. Well, it turns out your long history with viruses goes back much further.

Over our long evolutionary history many retroviruses have incorporated their DNA into our own genome. A retrovirus is a type of virus that inserts a copy of its genome into the genome of the host’s cells. It is thought that around 8% of our genome is composed of retroviral DNA. Scientists are just now discovering that these bits of viral DNA that were inserted into our very early ancestor’s cells millions and millions of years ago may not just have been passively riding along but also appear to make proteins that are important for certain cellular functions.

Researchers at the University of Utah Health who were investigating a protein called Arc made the shocking discovery that Arc originated from an ancient virus. The protein Arc has been determined to be essential for long-term memory in mammals. So, viruses are not only good at making you sick, but a long time ago they also provided us with a protein that is necessary for long-term memory. So, if you remember a person’s face, a phone number, your parent’s names, or where you live you may owe it all to an ancient virus.

Dr. Jason Shepperd, the primary researcher in the lab that published this shocking discovery, explains in an interview with Neuroscience News and Research that this discovery all started when they observed the structure of the protein under a microscope. They discovered that multiple copies of the Arc protein formed what looked like the protective shell of a virus, which is called a capsid. This finding was so shocking to the lab at the University of Utah Health when they first observed it that Dr. Jason Shepperd recalls thinking “What the hell is going on?”.

This shocking discovery that the structure of the Arc protein looked like a virus capsid led Jason and his team to analyze the history of the Arc protein across a wide range of animals to help track its evolutionary origin. They found that Arc protein is present in all tetrapods (mammals, birds, reptiles, and amphibians), but is absent in fish lineages. Also, interestingly, Arc is also found in all fly species, but due to differences in its genetic structure it appears to have evolved separately from that found in tetrapods. These findings suggest an ancient retrovirus ancestor as the origin for this proteins formation, but also that there were two events during which a virus infected both tetrapod ancestors around 350-400 million years ago, but also a second retrovirus infected the ancestors of flies around 150 million years later.

The viral history of the Arc protein offered Dr. Shepherd and his team an explanation as to why Arc formed the capsid like structure but left many questions like “Does this structure have a purpose?” and “How does this structure relate to Arc’s function in memory formation?”. To begin answering these questions and others, these researchers tried isolating the Arc protein capsids from brain cells. In the process of isolating the capsids from the brain cells the researchers discovered that Arc messenger RNA was also being isolated. Arc messenger RNA is the little bit of genetic code that is copied from the DNA that instructs the cell to create Arc protein. Finding Arc messenger RNA in the isolated capsids suggested to the team of researchers that much like how virus capsids protect and transport the genetic information for the virus, the Arc protein capsid was carrying the genetic information for making more Arc protein.

Although fascinating, this still left the question as to why Arc would be doing this. The researchers, seeing the similarities between Arc and viruses, checked to see if the similarities continued. When viruses invade a host cell and replicate, the new viral capsids are released from the cell and are then transported to other cells nearby where they enter the cell release the genetic information they stored.

Jason and his team did several experiments looking at if Arc capsids are released from cells in the brain, but also if they are taken up by other cells after being released. Knowing that the Arc capsids contain Arc messenger RNA, they searched around a cell that produced Arc capsids to see if they could find Arc messenger RNA. If they researchers were able to find Arc messenger RNA outside of the cell, it would provide evidence that Arc capsids were being released. At this point it might not be surprising, but the team found out that Arc messenger RNA and Arc capsids were being released from the cell. To top it all off, the team also found that cells with the Arc gene removed, when placed near a cell that contains the Arc gene, start producing the Arc protein themselves.

This ancient viral protein in our genome can form a virus like capsid as well carry the genetic information to create more Arc protein between cells. These findings that Jason and his team recently published shed light on a new form of communication between cells previously only known to viruses, as well as suggest a function for Arc protein which is essential for long-term memory. Given our long history with viruses, and how much viral DNA we carry with us in our genome, this work suggests that the Arc protein may not be the only viral protein we carry with a function. This finding highlights the importance of investigating our own viral DNA more thoroughly, as it may not only hold the key to our long-term memory but much more.

 What’s growing inside your brain that’s giving you Alzheimer’s?

By Ben Yefimov, 2018 WSU Vancouver Neuroscience Student

Bacteria are everywhere. They are on our skin, in our gut, and even our brain. And they may be a contributing factor that leads to Alzheimer’s disease.

Alzheimer’s is a disease that strips you of your identity by deteriorating your memory, cognition, and behavior. This disease develops over years and becomes burdensome enough to affect your everyday tasks. Although there are many types of dementias, Alzheimer’s disease is the most common form that effects 60 to 80 percent of all cases. This disease is affecting more and more people in our society. However, there is no cure yet.

What are the key pathological characteristics of this disease? It has been known for years that the buildup of specific proteins leads to Alzheimer’s disease. The specific protein that is associated with this disease is called amyloid beta, which over time forms plaques in the brain that causes the brain tissue to shrivel and die.

However, the mere quantity of this protein build-up does not directly relate to the severity of the disease. Other factors are also at play. One other factor that is thought to contribute to the disease is inflammation. Previous research has demonstrated that neuroinflammation, the inflammatory response of the brain, is associated with early stage of Alzheimer’s disease. However, other factors that can lead to inflammation are bacteria.

Researchers at University of Bristol in the UK wanted to see whether specific bacteria contribute to the development Alzheimer’s disease. Their aim was to use a novel DNA sequencing technique to look at the bacterial populations in human brains that had Alzheimer’s disease and normal, healthy brains. Using this technique allowed the researchers to extract DNA from the brain, including the DNA of bacteria that lived within the brain, and compare it to databases of bacteria. The importance of this technique is that it allowed for identification of unknown bacteria and low levels of particular bacteria. This was like finding invisible needles in a haystack, the haystack being the actual human brain DNA.

The study determined that there is 5 to 10 times more bacteria in the Alzheimer’s brains compared to the control, healthy brains. The two specific species that are contributing to this drastic bacterial increase are Staphylococcus and Propionibacteriaceae (P. acnes) bacteria. P. acnes bacterial species is found on human skin and mouth. However, it has been observed to negatively affect patients after operations and patients with chronic inflammatory diseases.

This study has determined that there is more P. acnes bacteria in Alzheimer’s brains compared to healthy bacteria and that the P. acnes bacteria can activate the immune response in patients. The bacteria are able to do so by releasing chemical signals that eventually lead to inflammation.

So how do these bacteria get inside of your brain and potentially lead to Alzheimer’s disease? Researchers believe that the bacteria enter the brain as a secondary infection, which initiates the start of Alzheimer’s disease.  The primary infection could have originated from an infection of the mouth, for example 15 to 20 years before the patient’s death. More research must be performed before we can for sure say that this devastating disease arises from infestation of unwanted bacteria. If the bacteria does cause the disease, we will have a clear targeted approach to treating patients with the disease and eventually finding a cure.

 Playing ‘Fact or Fake’ with Fibro

By Dyana Novicio, 2018 WSU Vancouver Neuroscience Student

If you Googled ‘what is fibromyalgia?’, the first link that appears is from WebMD. If you read what’s on the page, you’ll see that fibromyalgia (fibro in this piece) is described as “misunderstood” and “misdiagnosed”. Doctors don’t know what causes it either.

What we do know is that 2-4% of the population have been diagnosed with fibro and I’d bet anything most would love to be understood and determine the cause.

But first: What is this oh-so-mysterious fibro-thing?

Well, it literally means “muscle and fibrous connective tissue pain”. Doesn’t sound too bad, right?

Wrong — oh so wrong.

Imagine this: You wake up and immediately feel like you’ve only gotten a few hours of sleep. You’re sure you got 8 ½ hours of sleep, so why the achiness? Why the fatigue? You’re rushing to get to where you need to be but you can’t forget to take your depression medications. You also have terrible IBS so be prepared to feel like you “gotta go” all day. You down 3-4 times the recommended dosage of over-the-counter pain relief drugs for constant headaches and random pains all over your body. You struggle to concentrate on seemingly simple tasks or forget what you were just doing. You finally manage to get through the day but it’s a coin toss on whether you’ll “sleep” for 8 ½ hours or fall asleep in the first place.

Now imagine these symptoms happening 75-90% of your life for years. Sometimes, for years and years without ever getting an answer as to why because 1) all your lab workups are great. There’s nothing wrong with you. And 2) You’re not a crazy hypochondriac.

All the issues in our imaginative scenario above mimic the symptoms of many autoimmune diseases but never test positive so how can you diagnose a non-diagnosable condition? It’s certainly not a cookie cutter differential where doctors can take a sample of your blood and look for the “fibromyalgia-causing agent”. I mean, the best we’ve got for explaining the main symptom of fibro, the widespread body pain, is something called ‘central sensitization’. It’s essentially a phenomenon where pain processing neurons in the brain continue to send pain signals even if what’s caused the pain was completely benign. Thus, patients with fibro continue to have chronic pain because the brain can no longer discriminate between real pain or “fake” pain.

Why does the brain do this? Researchers in a pilot study suggest it is an interplay between peripheral nerve fibers and the constant hyperactivity of these pain neurons. By experimentally manipulating rats to produce extra excitatory brain chemicals in brain regions associated with pain, the researchers were able to observe decreased nerve fiber density and length in the rats’ hind paws. (It is important to note that there are studies observing this exact trend in fibromyalgia patients and their nerve fibers.) What this means is that the dysfunction in the brain could impact the physiology of structures far away from the brain. Even better, what this means for those with fibro is that we may have found a cause for the pain described in terms like “brain dysfunction” rather than “it’s-all-in-your-brain”. This is great news considering early studies suggested a purely physical cause for fibro such as damage to the tissue that encases the muscles. For the rest of the symptoms (IBS, sleep and mood disruptions) though, there is much to be studied.

Luckily, scientists from Europe have been using an early mammalian model of “fibro-like” rats to examine the effects of medications generally prescribed for fibromyalgia. These rats harbored observed characteristics of those with fibro in their muscles, brain and spine. The rats had reduced number of brain chemicals responsible for pain inhibition as well reduced muscular pressure thresholds. They found that fibro medications do increase pain thresholds but act differently in the spinal cord. Scientists aren’t sure why but it’s all we could ask for when it comes to fibro.

We may never know why but at least there’s research being done. Maybe it could give some of us hope.

 Are you predisposed to incurable blindness?

 By Alina Chizh, 2018 WSU Vancouver Neuroscience Student

Global Stem Cells Group  http://www.stemcellsgroup.com/guidelines-for-stem-cell-research/

Global Stem Cells Group http://www.stemcellsgroup.com/guidelines-for-stem-cell-research/

What if I told you that, 10 years from now, you will be blind? I’m sure many of us reading this would scramble to ask: Why? How? Is there a way I can prevent this? Is there a car accident I can avoid or a healthier lifestyle I can implement? “No” is the answer. A short, heart-stopping, irreversible “no.” This would be the reality of a person with retinitis pigmentosa.

Retinitis pigmentosa (RP) is an inherited disease. Most of the people with RP develop the disease because of gene mutations that can occur in just one of about 50 (or maybe more) genes. These mutated genes are supposed to have the book of instructions on how to make the proper protein food to feed the specific cells of the eyes, called photoreceptors. But because the genes are mutated, they decide to ignore that instruction book and don’t make the necessary proteins. When the photoreceptors don’t have enough of the right protein, they start losing their ability to function.

So now what? You inherited these lazy genes that don’t want to do their jobs, so the poor photoreceptors are dysfunctional and you become blind. Unfortunately, you can’t do anything to save them for the time being, but (there’s always a but) researchers are coming up with treatment possibilities and potential cure ideas.

Dr. Mark Humayun is an ophthalmologist and engineer from the University of Southern California (USC) that has worked with a company called Second Sight to create a prosthesis device for patients with severe RP. This device is called Argus II and it consists of 2 portions: a pair of glasses with a video camera, and a prosthesis implanted on the eye. The camera can wirelessly transmit visual information to the prosthesis and bypass the dysfunctional photoreceptor cells, and send the video to your brain. This process, while it does work, doesn’t give you the most accurate visual information, and you would only see large letters or objects, not that small text on your cellphone. But I would like to think of this device as just a temporary “appetizer” before the main meal: a cure to retinitis pigmentosa.

As always, there are several options for the “main meal,” and likewise, there are various types of potential cures that are currently being tested on RP patients. One option off the main course menu is the use of stem cell transplantation. This is the idea that you replace your old, starving photoreceptors that don’t have enough protein, with these new and healthy stem cells to do the job for the old guys. While there are three different categories of stem cells, adult stem cells have been showing some promise. A study done by researchers in Turkey have found that a specific type of adult stem cell that is derived from bone marrow called a mesenchymal stem cell was transplanted into the eyes of 11 patients. Out of these patients, 3 of them were able to see brighter colors and had better vision after the transplant. Although it seems that we are still far away from a cure, these baby steps towards our goal will undoubtedly lead to a breakthrough.

I bet if I asked you: “what would be the worst sense to lose?”; many of you would reply with “eyesight”. However, when you inherit a condition like RP, it’s not exactly preventable because it’s in your genes. But with current stem cell research for RP, there can be a change in the RP battle. Perhaps in 10 years, that heart-stopping, irreversible “no” could be changed to a “yes.”

 Running your mind

By Lorina Tomceac, 2018 WSU Vancouver Neuroscience Student



Have you ever wondered why you can’t fully function properly when under pressure, like thinking you forgot your car keys after you had just placed them in your pocket or purse, or looking for your phone while talking on the phone? I’m definitely guilty of such occurrences and I have a feeling I’m not alone. Well there is a possible culprit for such odd behavior.

It is stress. We hear about it often and experience stress on a daily basis whether it happens due to sleepless nights, pressure at work or family problems. There are two types of stress the body experiences, acute stress which is immediate, and chronic stress which is stress that is continuous and lasts for an extended period of time. Acute stress is beneficial; it is the body’s natural mechanism of response to unexpected events and allows the body to cope with the unexpected anomaly in order to restore stress levels back to normal. However, chronic stress is repeated exposure to a stressful situation which induces changes in the body that are detrimental.

Typically, the human body will counter stress with the release of a chemical known as cortisol. The prolonged increased level of this chemical in our body causes some changes in different parts of your brain. The two parts of the brain that are most affected are the hippocampus and the amygdala. The two systems regulate levels of emotion and the effectiveness of your memory. Our hippocampus can be thought of as a series of sticky notes stuck to our brain which reminds us of the things we have to do and how to do them and the amygdala in some way sorts them out and keeps the important ones while disposing of the least important notes.

Elevated cortisol levels in the body present for an extended period induce abnormal changes in the system. The amygdala starts messing up and does not know which sticky notes to keep and which to dispose and the hippocampus can no longer collect the sticky notes that remind us of what to do. The brain cells in the hippocampus shrink and become smaller, the number of those cells are reduced, and the cells that are present stop working as efficiently. Research done in rats shows that the hippocampus is especially sensitive to elevated levels of cortisol in the body. In the study the researchers analyzed the effects of chronic immobilization stress and chronic unpredictable stress in rats. Through morphological analysis of hippocampal cells, they observed that the hippocampus in chronically stressed rats was more vulnerable to degenerative changes which included both shrinkage of the cell and reduction in number of cells present. The prolonged exposure of cortisol impairs the body’s natural coping mechanism and leads to many complications such as memory impairment and development of psychiatric disorder such as depression and anxiety.

Chronic stress also causes changes in the amygdala, the almond shaped gland in your brain that regulates your emotions. A recent study done in rats showed that the amygdala volume increased over time when the rats were exposed to unpredicted chronic mild stress, causing enhanced activity and connectivity in the system. Enhanced amygdala activity results in enhanced emotionality which can lead to development of disorders such as phobias, depression, and anxiety, and it also impairs cognitive reasoning. As you can see chronic stress is a major problem because your memory is impaired making it much more difficult for you to remember recent events or concentrate on a specific memory or learn something new, and your emotional response is enhanced causing you to overreact to stressful situations. Now you know why you can’t function properly when under pressure or in a stressful situation. The good news is there are ways we can reduce the damage.

In a recent study published in the journal of Behavioral Brain Research scientists observed that when chronically stressed rats exercised, the damaging effects of chronic stress were reduced, more newborn cells in the hippocampus survived and the cells worked more efficiently enhancing cognitive function. A similar recent study also done in rats showed that swimming reversed depression like behaviors induced by chronic unpredictable mild stress which was also correlated to the changes occurring in the hippocampus when body is exposed to chronic stress. Therefore, there is hope, although we can’t control the occurrence of stressful situations in our lives, we do have control over how we react and cope with it. Take control of your stress before it takes control of you. It can be as simple as starting your day with a jog or a few laps in the pool instead of the usual cup of coffee or morning news feed.

 The Study of Estrogen in a Local Research Lab

 By Jordan Hiblar, 2018 WSU Vancouver Neuroscience Student

In health class most of us learned that estrogen is involved in the female reproductive system and testosterone is involved in the male reproductive system. But what most of us didn’t learn is that estrogen also has many effects in the female brain not typically discussed. This is the primary focus of Martin Kelly’s research lab at Oregon Health and Science University (OHSU).

Researchers here examine estrogen’s effects specifically on homeostasis within the body and various other behaviors, such as food intake. Homeostasis is the body’s way of maintaining balance in all of its systems. An example of this is regulating body temperature-something estrogen happens to play a large role in. This is seen most notably in menopause when women experience hot flashes.

Estrogen can also alter behaviors such as eating, and more specifically how much of a good tasting food they are eating, like something high in sugar or fat. Estrogen has also been shown to have effects on anxiety levels in females. In the Kelly lab, they use mice to study these effects estrogen has on the female brain.

Kelly’s research is significant because the female brain is severely under studied in neuroscience. This obviously is a large problem because females are not biologically the same as males and can have a profoundly different response to various drugs or other stimuli in their environment.

Jordan pic

This graph shows how estrogen levels vary in human females over a month. In female mice these changes happen over 4-5 days instead of 30. This creates an uncontrolled variable in experiments. https://www.webmd.com/women/pms/ss/slideshow-premenstrual-syndrome-pms

One of the biggest reasons that female mice are difficult to study is that their estrogen levels within their system change very quickly. In humans, estrogen levels go up and down on a monthly cycle, however in mice, this cycle is 4 to 5 days instead of 30 (Fig 1). This means that to study females, experiments would have to be completed quickly because if there are different estrogen levels in a mouse over the course of an experiment, it presents an uncontrolled variable that could have an effect on the results. This means that more research needs to be done to greater understand the effects of estrogen.

To deal with this problem, researchers control estrogen levels within the mouse by removing the ovaries, essentially stopping estrogen release within the mouse. They then are able to give the mouse as much or as little estrogen for as long or short as they’d like in a lab setting.

Using these techniques, the researchers observe how much the female mice eat, their anxiety levels, and motivation. By studying the different effects estrogen has, Kelly and his colleagues hope to be able to slowly balance the scientific work done on females and add to the lacking body of knowledge on estrogen.


A Universal Building Block to Humans

Eric pic By Eric Polch, 2018 WSU Vancouver Neuroscience Student

If you were to buy a Lego set you’d expect that when purchasing it, all the pieces would be there. There’s also the notion that each piece in that set is matching color wise. But when you start building this set, you realize that some of the critical Lego blocks are missing! These are the type of circumstances that children with Autism Spectrum Disorder could experience.

Autism Spectrum Disorder (ASD) is a developmental disorder that is diagnosed in several categories ranging from dysfunction in social behavior to autoimmune system abnormalities.   Current statistics show that 1 out of 166 children could develop ASD; even more striking is that boys are nearly five times more likely to be diagnosed with ASD compared to girls.

The behavioral symptoms can range from irregularities in speech, socializing and maturing. Making matters even worse, is that the child’s own immune system could contribute to the development of ASD. Recent animal research has associated certain autoimmune inflammatory symptoms to behavioral symptoms, similarly found in ASD. This study was testing the hypothesis of autoimmunity-associated behavioral syndrome (AABS).  Experimental mice developed lesion within their G.I. tract and were behaviorally assessed through a water-maze experiment. When compared to the controls, the autoimmune mice had impaired psychomotor response.  The lesions were caused by chronic inflammation signals and led to noticeable difference in adaptive behavioral responses. This data established findings that particular brain-reactive antibodies, also known as cytokines could be related to ASD symptoms.

Clinical review studies then proceeded to look at the correlation between G.I. symptoms and ASD in children. In those studies, approximately 24% of the 2973 surveyed ASD patients had at least one symptom in relation to their G.I. tract.  Another study reported that ASD children were six to eight times more likely to have symptoms like irritable bowel syndrome (IBS). Symptoms like IBS, involve intestinal inflammation that’s caused by the same brain reactive antibodies seen in AABS mice study. These clinical studies established that development of ASD could involve a buildup of pro-inflammatory cytokines in the body.

At this point, the whole Lego Set could be compromised, but what if there was a way to get those missing pieces back? What if that missing piece could fix the autoimmune symptoms of ASD? In 1960 Alexander Friedenstein extracted bone marrow cells to study their multipotent nature. These mesenchymal stem cells (MSC) were shown to be a precursor to other specialized cells, such as the immune system. With current technology, MSC’s can be mass produced for treatment involving the immune system, tissue damage and regeneration.  These advances have led research to believe that MSCs could be used to regulate the autoimmune symptoms in ASD. In vivo & in vitro studies showed that MSCs inhibited the buildup of cytokines. Now clinical trials are starting to examine how effective MSC can be at treating the autoimmune symptoms of ASD. Much like having the basic building blocks for Lego, MSCs are the Lego blocks of the human body. In terms of the circumstances of ASD patients, MSCs can be answer to their autoimmune symptoms.

 Life Changing Treatment for Multiple Sclerosis

By Dhruv Sharma, 2018 WSU Vancouver Neuroscience Student

Imagine you suddenly can’t button up your shirt, you can’t tie your shoe, and pouring your morning coffee becomes an impossible task. Imagine, along with all of this, your body is constantly cramping, along with feeling tired and weak. I’m pretty sure right now you must be thinking that if this scenario was real, your life would be a living nightmare. Unfortunately this nightmare is a reality for many people who suffer from Multiple Sclerosis (MS). It is estimated that approximately 400,000 people in the United States are affected by MS. Despite its prevalence in many North American and European countries there currently is no cure that has been discovered.



MS is classified as an autoimmune disease due to the fact that it occurs when a person’s immune system attacks their healthy cells. The role of the immune system is to fight off infectious bacteria and viruses in a person’s body. In the case of MS, the immune system begins attacking the central nervous system, specifically the myelin. The myelin is a fatty substance that surrounds neurons. It plays a role similar to an insulator that wraps around a copper wire. Through this, the myelin is able to improve the neuron’s ability to send signals all across our body. When the immune system attacks the myelin, the damage diminishes the neuron’s ability to send signals to the body. When this occurs the patient may experience a wide range of symptoms ranging from vision loss to impaired hand eye coordination.

Although there is no cure for MS, there are many effective treatments used by physicians.  The two main treatments for MS include the use of physical therapy and immunosuppressant drugs. These drugs work by slowing down the activity of your immune system, in order to prevent it from attacking your neurons. Although these treatment methods have shown to be effective in treating the disease they do have some drawbacks. For example, although immunosuppressant drugs are able to prevent the immune system from attacking the nervous system, they are not able to rebuild new myelin around neurons. This causes patients, who have neurons with damaged myelin, to have no symptomatic improvement.. Due to this, current treatments only offer a way to slow down the progression of MS, and are not successful in reversing its effects.

In order to address this problem, neuroscientists have begun developing a new method for treating MS known as Remyelination therapy. The goal of this therapy is to rebuild the myelin around damaged neurons in order to restore their proper functioning. This works in a similar manner to attaching an insulator to a wire in order to protect it. For this to work, oligodendrocyte progenitor cells (OPCs) are required to rebuild myelin around damaged neurons. OPCs have the unique ability to rebuild the myelin around neurons after they have been damaged. Current research is focusing on ways to help promote activity of OPCs in MS patients. In fact, some studies have found that this therapy is effective in repairing and rebuilding the myelin around neurons.

Remyelination Therapy has the potential to transform the lives of millions of people suffering from MS. Any new breakthroughs in research may one day allow damaged neurons to rebuild their myelin and allow them to communicate effectively with other cells. If this occurs then individuals suffering from MS will once again gain the ability to easily perform their day to day tasks, and actively enjoy their lives.

Gut Feelings: How bacteria in your gut have a direct impact on your mood and personality

By Bradley Dowling, WSU Vancouver Neuroscience Student

At this very moment, there are roughly 30 to 40 trillion bacteria living inside your large intestine. 30 to 40 trillion. There are more bacteria living along the walls of your gut than there are cells in your entire body. This is your gut microbiome. It’s an absolutely vast array of nearly 1000 different species of microbes living in harmony with each other, all negotiating for a limited amount of space and resources. Surprisingly, the gut microbiome would barely be able to fill a small soup can. That doesn’t change how important these little critters are to us. These bacteria help us digest our food and protect us from more harmful microbes that could cause disease. More importantly, they train our immune system to tell the difference between good microbes and the bad ones. If our body reacted to every single microbe it encountered, we’d never stop being sick. Instead, we only react to the ones that our body knows are dangerous. But the gut microbiome’s influence doesn’t stop at our immune system. Instead, its reach extends directly to our brain and surprisingly, our mood.

How could bacteria in your gut have an impact on your mood? The answer lies in what scientists call the Gut-Brain Axis, or the communication between your brain and your gut. The brain talks to your intestines, telling it when to digest foods and when not to, and helps direct the movement of food along the digestive tract. This communication is not one way, and it isn’t just your intestines that respond to the brain’s play-calling. Amazingly, bacteria can talk back as well, and appear to play a part in brain development and activity in ways that have only recently been uncovered.

Recall that the good bacteria in your gut help to tune your immune system. Too many of the bad bacteria and too few of the good ones can lead to an over active immune system, which can be harmful to your brain and cause depression, anxiety, and memory problems, and is potentially linked to disorders like Autism. The connection between these disorders and the microbiome is strong. More than 50% of people with irritable bowel syndrome also have symptoms of depression, and children with Autism are 3.5 times more likely to suffer from chronic GI problems than children without Autism. The good news is that you aren’t stuck with the gut bacteria you have right now. Amazingly, scientists have found that switching the gut bacteria between two different species of mice through a process called fecal transplant effectively switched their personalities. Fecal transplants are exactly what they sound like. Scientists take the feces of one animal (or human), and insert them into the bowels of another. This works especially well in ridding the gut of harmful bacteria like Clostridium difficile, the hard-to-remove organism in the large intestine that is responsible for colitis.

Don’t worry though; there are easier and less disgusting ways for you to alter your gut microbiome. Currently, there is a lot of research being performed on probiotic supplements that could have a beneficial impact on your mental health. Think of probiotics simply as beneficial bacteria either in a capsule or in your food. Scientists call this new class of probiotics ‘psychobiotics.’ The research is new and promising but ultimately, the best thing you can do for your mental health right now is eat a healthy diet. Surprise, right? Changing your diet can have a profound impact on the bacteria in your intestine, because the food that you eat is also the food that they eat. So, if different bacteria can have different impacts on your brain and your mood, and your gut bacterial populations can change, can you improve your mood simply by eating more of the foods that healthy bacteria eat? The answer is yes! The majority of healthy beneficial bacteria in our gut feast on fiber, the material from whole grains, fruits, vegetables, and nuts that you cannot digest on your own. The problem is that most Americans simply don’t have enough fiber in their diets. According to Dr. Justin Sonnenberg of Stanford University and co-author of the book The Good Gut, the typical American only gets around 15 grams of fiber in their diet per day. In contrast, our very recent ancestors in hunter-gather societies ate approximately 10 times that amount. Depriving your beneficial bacteria of this much food is effectively starving them off to make way for more harmful bacteria or worse, forcing them to feed off of the mucous lining in your gut that protects your intestines and body from the outside world. Dr. Sonnenberg recommends getting between 30 and 60 grams of fiber every day to help nourish a diverse gut microbiome. Doing so will ensure that the beneficial bacteria in your gut can flourish, and keeping your bacteria happy will go a long way in keeping you happy. After all, good food is much more appetizing than a fecal transplant.

Wait doctor, have you consulted your computer yet? The future of epilepsy treatment

By Joseph Seuferling, WSU Vancouver Neuroscience Student

You are walking your dog through the park on a beautiful sunny day with tennis ball in hand ready for an afternoon of play time with man’s best friend. The smell of flowers and the view of an open green field draw you further into the park. Removing the leash from the collar of your furry friend, you draw back and toss the tennis ball into the field as your dog dashes away for his favorite toy. Your dog quickly runs back to you and returns the tennis ball from his mouth dripping in saliva. After wiping your hand on your pant leg, you reach to pat your old friend on the head and he enjoys the attention. Suddenly, you fall to the ground shaking uncontrollably; the sunny clear skies begin to fade black as your eyes fall shut and you lose consciousness. What happened? Why did the story end on such a sudden note?

Imagine this happening while leaning in for your first kiss or when performing on stage for a crowd. A person living with the neurological disorder epilepsy may have the end of many stories decided abruptly for them every day. Epilepsy is characterized by random and sudden episodes of uncontrollable and irregular shaking of the body and possible loss of consciousness; these episodes are typically called seizures. A person might have one seizure their whole life, but for this with epilepsy the seizures never end.

Many patients are able to manage their epileptic seizures with one of many medications prescribed for the disorder, which prevent seizures by blocking increased neuron activation or increasing neuron inhibition within the nervous system when a seizure occurs. Unfortunately, many patients with epilepsy are unable to alleviate their seizure symptoms with these medications. You’re probably wondering what alternative treatment options these patients have, are they cursed to live with seizures their whole life? Do not despair, epileptic patients have the final option of brain surgery! Why would you want someone sticking their hands in your brain?! Surgical intervention could create seizure free life for epileptic patients, but it is not always successful. Brain surgery performed today, such as a lobectomy which is completed through removal of an area of the brain where a patient’s seizures originate, has been inconsistent in decreasing seizure occurrence. Neurosurgeons continue to use the lobectomy procedure to remove the same region of the brain for epileptic patients. The saying “One size fits all” describes medical decision making for modern day epileptic neurosurgical treatment. Epileptic patient’s brains are affected by epilepsy differently depending on each individual, and they have variation in regions most prone to seizure activity.

A new approach must be taken from the promising subfield of neuroscience, termed computational neuroscience, which utilizes advanced technology such as computer modeling, imaging, and simulation to efficiently compile complex information of the brain. In a recent study conducted by Frances Hutchings et al., researchers used computerized brain imaging and simulation derived from the sub-field of computational neuroscience to specifically improve epileptic surgical treatment. They took images of epileptic patient’s brains and created a computerized 3D model; with similar 3D graphics seen in your favorite Pixar movie!

The researchers named each region of the computerized brain associated with epilepsy a “node”, like marking regions with a big red flag, and stimulated the nodes with electrically simulated noise, or oscillation frequencies. The noise frequencies simulated seizures in the 3D brain model and nodes or brain regions most effected byJoey pic1 seizure activity reacted to frequencies the fastest. The scientists then removed nodes in the 3D simulation, representing live surgical removal of brain regions. They removed node or brain regions most commonly taken from patients undergoing a lobectomy, then nodes most quickly effected in each individual patient, specific to their brain. The researchers found that simulated brains with most effected patient specific nodes removed presented with 100% improvement of seizure activity whereas the common lobectomy node removal demonstrated only 72.7% improvement after seizure simulation. This computationally inspired method of neurosurgical treatment may allow physicians to conduct personalized surgical treatment that more successfully decreases seizure activity compared to the “One size fits all” lobectomy of the same brain region in each epileptic patient.


You now awake in the bed of your nearest hospital, your furry friend licking your face. Your physician explains that you just had an epileptic seizure. They describe surgical intervention as a treatment option and how they are able create a computerized model of your brain to accurately remove regions causing your seizures. A future where medical professionals are able to make such informed decisions concerning neurosurgery would have greatly improved epileptic treatment, as physicians might then have the ability to prevent your wonderful life stories from ending so abruptly due to seizures.

The pedophiles among us

By Hannah Turner, WSU Vancouver Neuroscience Student

Pedophile. The word alone incites a whirlwind of emotion and anger. It is likely that pedophiles are the most detested population that function within our society… But who are these people that walk among us?

Pedophiles are thought to make up at least 1% of the general population. The disorder is characterized by an exclusive or primary sexual attraction to prepubescent children. The definition itself can actually allow us to dispel some common misconceptions. Although pedophilia is often thought of as being synonymous with child molestation, less than half of reported sexual offenses committed against children are committed by pedophiles. So, who are committing these crimes? The largest population of people who sexually abuse children do so because the opportunity arises – they are often close family friends or even family members of the victim. This group of non-pedophilic offenders tends to use children as substitutes for adult partners, but they are not preferentially attracted to children. This means that not all pedophiles are sex offenders and the majority of offenders are not pedophilic.

Hannah pic1The abuse of our youth is a disturbing epidemic. It is now estimated that 1 in 10 children become victims of sexual abuse before they reach the age of 18. Whether you recognize it or not, someone you know has likely experienced childhood sexual abuse. It is easy to feel angry when digesting statistics like this, and although the issue of pedophilia is emotionally charged, scientists are striving to understand the causes of this disorder. With a growing body of research on pedophilia forming, a biological profile has slowly been coming together. It is estimated that nearly 30% of pedophiles are left handed, which is about three times the rate seen in the general population. As a group they are notably shorter and have a lower IQ compared to the average person. When we dig even deeper and look at imaging of their brains, we see striking differences – the pedophilic brain is actually smaller in certain regions compared to the average person. One example of this is the orbitofrontal cortex, which is thought to be responsible for cognitive processing and decision-making. When presented with pictures of children, these brains illicit a similar sexual response to what is seen when control groups are processing pictures of sexually attractive age appropriate partners.

This biological profile currently being developed by scientists points towards a genetic basis for pedophilia, meaning that it is likely not a disorder that can be cured. With the knowledge that pedophilia is seemingly innate, the focus of research has shifted. Researchers are now designing experiments that could elucidate better treatments for the condition. These treatments generally aim to enable someone to resist acting on sexual urges. More effective treatments for the disorder would mean lower rates of offending and reoffended and in turn less children being sexually abused.

Most recently, researchers have been working to identify differences between offending and non-offending pedophiles. A more complete understanding of what differentiates these groups would allow for the development of treatment methods that could be tailored to an individual’s behavior. These methods would aim to prevent reoffending or prevent pedophiles from progressing into perpetrators altogether. A recent study looked at the brains of offending pedophiles while they were completing tasks associated with impulse control and compared those results to the brains of non-offenders. During the performance of these tasks, non-offending pedophiles seemed to be employing additional pathways in their brain to allow for greater self-control. These findings suggest that treatment and therapy aimed at developing greater control abilities in pedophiles could help prevent offences.

The emotion surrounding pedophilia is certainly warranted, but in many ways it has prevented those struggling with the disorder from accessing resources and getting much needed help. Although there is a population of non-offenders struggling to control their urges, it is a difficult and lonely existence where one slip-up could destroy a child’s life. The stakes in these situations are too high and we can no longer ignore their needs for treatment. By finding a way to dissociate the emotion surrounding pedophilia and the treatment of this condition clinically, we can protect more children and prevent more instances of childhood sexual abuse.

Opioids: Paging Dr. Feel-Good

By Andrea Lee, WSU Vancouver Neuroscience Student

On April 21, 2016, Prince’s sudden death made the headlines of every major newspaper.  Every media outlet was reporting 24/7 about the music icon’s tragic death in his Paisley Park recording studio in Chanhassen, Minnesota. What they weren’t talking about was that deaths like his are becoming common. In a two week period prior to Prince’s untimely death, there were 42 overdoses and 10 deaths in Sacramento alone.   Sadly, Prince was just one of many victims of drug overdose.

The growing opioid epidemic ripping through the United States has caused almost 100 deaths per day according to CDC as of 2015 and has only accelerated since then. Opioid use, prescription or otherwise, permeates every corner of America. According to the CDC, 47,055 drug overdoses death were reported in 2014 of which 61% (28,647) involved some type opioid.  How did this happen?  How did daily Opioid overdoses quadruple in just over a decade?

We all have experienced pain.  Some pain, like a stubbed toe, goes away after a couple minutes and others, like those from a serious car accident, persist for a longer period of time and become known as chronic pain conditions (e.g. joint pain, backache, or muscle & nerve pain).  Almost 30% of Americans suffer from a chronic pain condition  making it impossible to live a normal, pain free, life.  The number one treatment for chronic pain is opioids (e.g. fentanyl, methadone, morphine etc.).  Opioids have a great advantage because they relieve pain almost immediately. In 1992, Health secretary Lewis Sullivan stated that it is a “myth” that painkillers are addictive.  It is no surprise that they have become the most commonly prescribed medication in the United States?

The benefits of opioid treatment against pain are questionable outside of the hospital setting. Moreover, we now know that it is not a “myth” that opioids are addictive; they are highly addictive and causing a firestorm of overdoses and deaths.  We need to do something about this epidemic now, before it gets worse but what can we do?

The Laboratory of Dr. Michael Morgan at Washington State University, Vancouver, is working with lab rats to answer just that question.  To a lab rat, wheel running is a normal and enjoyable daily activity.  By monitoring changes in this activity as opioids are introduced and removed, they are able to determine how opioid use affects behavior.  Andrea Lee, an undergraduate who is conducting the study explains, “In order to know how we can help those who’ve become addicted to opioids, first, we need to understand the effects of opioids on the body and how those effects can turn negative or deadly as they leave the body.”  She continues “Once we fully understand the process we can develop a treatment protocol to help people move from addiction to being drug free or, more optimistically, to develop drug protocols that avoid addiction entirely.”

Changes in brain matter during pregnancy…is there a link to post-partum depression?

By Laura Kays, WSU Vancouver Neuroscience Student

Many women experience forgetfulness, known as pregnancy brain, throughout and following pregnancy. Research published in Nature Neuroscience shows there are significant differences in the female brain before and after child birth.  The study looked at MRI scans before and after pregnancy in first time mothers. Researchers could tell from looking at the brain structure through an MRI which women had experienced pregnancy.  Pregnancy affects the hippocampus, which is the memory center of the brain.  Women’s memory and the volume of cells within the hippocampus return to normal following the post-partum period.  Regions of the brain that are involved in social cognition and social behavior also undergo remodeling during pregnancy. These changes predict a measure of post-partum maternal attachment. To support that these changes are associated with maternal attachment and not just being a new parent, researchers looked at MRI scans of first time fathers before and after the birth of their first child.  The change in brain structure that is seen in women does not occur in men.

The study published in Nature Neuroscience looked at brain images and how these changes are involved in cognition and attachment.  2 year follow up shows the persistence of these changes in brain matter.  The changes occur whether a women conceives a child naturally or by fertility treatment. The areas that undergo remodeling overlap with the theory of mind network (ToM).  ToM provides skills for thinking about the thoughts and beliefs of oneself and others. This allows people to make sense of the behaviors of others.   Functional MRI (fMRI) studies assess brain activity in response to different stimuli. Researchers looked at brain activity in women following pregnancy when shown pictures of their newborn baby as well as images of other babies.  The regions that are most active when a women views an image of her baby are the regions that undergo remodeling during pregnancy. The more distinct the changes are in women’s brain the higher she will score on maternal attachment measures. Two year follow up analysis shows no further remodeling is experienced and that there is no recovery in brain matter volume other than in the hippocampus compared to pre pregnancy measurements.  The hippocampus shows selective recovery after 2 years.

Changes in brain matter are correlated with post-partum maternal attachment.  Research published in Psychological Medicine shows how ToM can predict sensitivity in mothers with any mental health diagnosis. This study looked specifically at new moms with a mental condition, but found that no difference was seen in maternal sensitivity between healthy women and women with a mental condition. The lack of maternal attachment following child birth is a severe symptom of post-partum depression.  Post-partum depression is a complex and unpredictable condition that 1 in 7 women experience.  It is possible that remodeling of the brain during pregnancy does not occur in women who experience post-partum depression.  Further research could provide insight on what goes on in the brain of new moms who experience lack of attachment to their child. This research provides reason to explore better treatments and interventions to improve bonding between mothers and their babies when they experience post-partum depression.

The Silent Thief

By Imee Williams, WSU Vancouver Neuroscience Student

This is not an ordinary robber. They are eyeing one thing and one thing only. No, not your money or your precious jewels. No, not even that brand new 70” flat screen television you purchased for your birthday. This burglar is glaucoma and it wants your vision.

Glaucoma is the second leading cause of preventable blindness today, affecting more than 3 million Americans and over 60 million globally. This disease is associated with an increase in pressure inside the eye which damages the internal structure of the eye, leading to irreversible blindness. There is a nerve that connects the eye to our brain and allows us to interpret our environment. The buildup of pressure damages the eye’s tissue, nerve, and the fat that surrounds the nerve known as myelin. Without early detection this silent thief cannot be caught and will continue to steal vision for years.

I have some good news and some bad news. I’ll start with the bad news since that’s what I assume you’d like to hear first. There is currently no cure for vision loss and scientists still do not understand how this build-up of pressure even begins. Early signs of this disease cannot be detected because the earliest changes to the eye are not yet known. Today, Devers Eye Institute has a group of researchers working to figure out who is helping this thief and how to catch them before they steal every last part of your vision.

Now, for the good news! Dr. Claude Burgoyne and his colleagues are testing two possible candidates that might cause glaucoma: the “chewer” and the “traveler”. The eye is a complex system that consists of many cell types. Two in particular that have raised interest: oligodendrocytes and astrocytes. Let’s think of them as the builder and the janitor. The oligodendrocyte builds the myelin that surrounds the nerve and the astrocyte “chews up” any myelin that is damaged or needs repair. They make a beautiful pair when these two work perfectly. However, when the cells don’t communicate properly things can go horribly wrong. Some signal, which continues to stay a mystery, communicates to the astrocyte that it needs to chew up myelin, whether it’s damaged or not.

The back of the eye is composed of tissue called sclera. There is a hole located inside the sclera called the lamina, which is like an intermediate step before the nerve can reach the brain. In a healthy normal eye, the lamina assists the nerve to transmit signals effectively. In glaucoma, the increase in pressure inside the eye shifts the location of the lamina. The lamina literally packs up and leaves the nerve behind.

Both of these processes are found during early stages of glaucoma. Current research is tackling the infamous question, “what came first, the chicken or the egg?” Or is it a combination of the two? By understanding the underlying cause and process of the disease, we can design effective treatments and medication as well as detect early stages of glaucoma in a clinical setting.

Our eyes are important to perform tasks and engage in social interactions. Without our vision, our quality of life dramatically decreases. Glaucoma can have a life changing impact on anyone. It has puzzled scientists for several years, but they are beginning to reveal more and more about this devastating disease. It won’t be long before justice is served for this silent thief.

Therapy for your brain

By Kathleen Darling, WSU Vancouver Neuroscience Student

Anxiety affects all of our lives. We feel nervous about a job interview, an important test, or really anything that takes us out of our comfort zones. For many people, though, anxiety goes beyond a queasy feeling in the stomach, into full blown panic. This is a psychological problem known as Social Anxiety Disorder, or SAD. But it makes people who suffer from it more than just sad. The symptoms of social anxiety disorder often include stress and fear so debilitating that these people would rather stay home and risk their future success, than risk having a panic attack in public.

Such powerful chronic anxiety can make it hard to go through life, which is why many people seek out therapy as a means of treating anxiety. The most common type is known as cognitive behavioral therapy, or CBT, a newer method of psychological therapy. Far off the typical “and how does that make you feel?” we’ve all seen on television, cognitive behavioral therapists help their patients find ways to work around their anxiety, instead of claiming to remove or ignore it. So, where an old-school therapist might try to delve into the roots of your problems, CBT encourages patients to be more aware of their current mental state, and teaches patients ways of changing negative thoughts into positive actions. By this method, people suffering from anxiety disorders can always feel ready to react to their disruptive symptoms in a constructive way, and so not feel helpless the next time they feel like going out to a concert or chatting up a stranger.

We’ve known behavioral therapy is highly effective in treating anxiety disorders for decades now, but we haven’t known exactly how they affect our brains, until now. A new study, done at the Functional Brain Imaging Centre in Umeå, Sweden, used advanced imaging techniques to look at the brains of SAD patients who had undergone CBT. Using magnetic resonance imaging, or MRI, harmless magnetic waves can be used to scan the brain of conscious people, to obtain a full 3-D picture of the full structure, down to very small and specific parts.

The amygdala is one such small structure, located deep toward the center of the brain. It’s part of many of the brain’s basest functions, most fundamentally of which is the fight-or-flight response, often just referred to as the fear response. So you can see why this would be a place to point fingers at in dealing with anxiety disorders! Using MRI, a literal difference was seen in the size of the amygdalas of these patients. They appeared to be significantly smaller, by as much as 15%. That may not seem like much, but 15% is a big deal in the brain, where every single nanometer of space is budgeted precisely. So, a loss in mass that drastic leads scientists to believe that there is a decrease in the amount of time these amygdalas are being used, suggesting that CBT really has lowered the fear response for these people.

What’s even more intriguing, though, is how the change potentiates over time. You see, after a year of therapy, the Swedish research team went back and imaged the brains of the same patients again. These patients still had greatly lowered anxiety symptoms, confirmed by their therapists. However, the size of their amygdalas had returned to normal, functioning as though they had never been a problem in the first place.

This amazing discovery sheds light on the way therapy really functions in the brain. Researchers now believe that the brain has two states of anxiety disorder recovery. First, the amygdala undergoes a short term major physical change, immediately lowering the amount of the brain that is available to invoke fear and panic. Next, the brain goes through a long-term change, wherein the way fear is processed is reprogrammed, directed to the areas of the brain that allow for healthy and measured responses to stress, and so the amygdala can go back to its other, less harmful tasks.

It turns out, therapy really is just like any other medicine- keep taking it until your doctor says you’re done, not just until you feel better, or you may just be setting yourself up for failure in the long run!

Marijuana was the “high” way to my relief

Chronic pain is a debilitating condition worldwide, yet current therapies are limited by poor efficacy and many side effects. Doctors typically prescribe opioids for pain relief. Opioids include drugs such as morphine and oxycodone but heroin also fits in this category. These drugs are dangerous. More people die from drug overdose than from car accidents. Overdoes and addiction to opioids have us spiraling farther into this epidemic, in just 30 years deaths from opioid-related overdoses have quadrupled in the United States.

I went in for a knee surgery and was prescribed oxycodone for pain. One week after surgery, patients are supposed to start walking but I was unable. After the course of a month, I was still bed ridden and my pain went up exponentially, and with that so did my oxycodone dosage. I was taking three oxycodone every three hours and pain was still unmanageable. I had a complete loss of appetite resulting in a diet that consisted of 7 Ritz crackers a day. I lost 35 lbs., my cheeks had sunk into my face, and I was unrecognizable to my friends. Quickly things turned awry. I was unable to control my body temperature. It would fluctuate between 96  – 102  so I went to the doctors and blood work was done to help diagnose the problem. Later that evening when I returned home, I was lying in bed and the phone rang. It was my surgeon. He said, “Your blood work has come back and you have a life-threatening infection in the bones of your body. We need to perform emergency surgery in the morning”.  The next morning, I was wheeled into surgery.

After surgery, when I returned home, I was sitting in the recliner, looking at prescription bottles and thinking, “I can’t take another pill”. I should have mentioned that opioids make you constipated as shit. I hadn’t taken a good poo in about a month. So, I decided to self-medicate with marijuana. But this time, treatment was effective. In fact, I was so relieved of my pain I didn’t need to take another oxycodone pill. Until, one day, I started to feel weak again. I was so frail that I couldn’t support the own weight of my knobby, corpse of a body. When night came, I was afraid to sleep. I felt so frail that I thought if I got too relaxed, I would die, I picked up the phone and called my best friend, I told her to buy a plane ticket to come home because I didn’t know if I would make it through the night.

A nurse tried to take my pulse but it was too faint to get a reading on. It was determined that I was going through opioid withdrawal. The cessation of oxycodone was too great for my now warn-down and anemic body to endure, I had become dependent on oxycodone. If my doctor wasn’t educated on opioid withdrawal I don’t know what I would have done. He prescribed me another bottle of oxycodone so that I could slowly wean myself off. Unlike many stories, mine was a successful one.

I currently work in a lab to help these people. Opioid addiction and overdose is a serious epidemic that has swept the nation. My research asks if marijauna is a safer alternative to opioids. One of our research findings supports that the alternation of marijuana and opioids enhance their pain relieving effects. In a clinical setting this would be extremely beneficial. A doctor could prescribe marijuana with oxycodone. In doing this the doctor could lower the dose of oxycodone prescribed and lower the chance for developing an addiction or dependence. Marijuana is a great prospect drug because it is relatively not addictive and has no lethal properties. Marijuana provides a safe, effective, and affordable treatment option for the millions of people suffering from chronic pain worldwide.


Magnets make you “you again”: How altering brain waves improves cognition after brain trauma or disease

By Erin Cooper, WSU Vancouver Neuroscience Student

Source: NASA Astronomy Picture of the Day

Source: NASA Astronomy Picture of the Day

When you look up at the clear night sky, you can see countless stars, suggesting the vastness of our universe. Scientists and mathematicians speculate there are more connections in our brain than there are stars in the universe. There are an estimated 87 billion neurons in the human brain and each one has the ability to connect with a varying number of other neurons. In life, it is the personal connections and daily interactions that give life meaning; this is also how the brain works. The interactions between neurons shape your personality and your unique perceptions. But what happens when disease or trauma to the brain breaks these connections? Interactions are lost. Personalities, memories, comprehension, and other complex mental processes are lost.

The Brain Treatment Center in Newport, CA., specializes in strengthening connections that are left after trauma and disease has taken its toll. In patients with post-traumatic stress disorder (PTSD), traumatic brain injury (TBI), autism, major depression, and anxiety, large circuit connections are interrupted and parts of the brain no longer communicate properly. The characteristics of these lost connections are seen as symptoms in the patient or they can be visualized by using a noninvasive medical technique that records brain waves called the electroencephalogram. Patients with anxiety and PTSD tend to have higher energy Beta waves and patients with TBI tend to have lower energy Delta and Theta waves. Analysis of these waves identifies areas of the brain that do not function properly due to disease or trauma. The Brain Treatment Center uses an old technique with a new twist to alter brain waves. Magnetic resonance therapy with electrocardiogram (MeRT) uses transcranial magnetic stimulation (TMS), a device that generates magnetic pulses to generate electricity in the brain. Unlike TMS, MeRT tailors treatment to the patient’s brain and it incorporates an electrical recording from the heart via electrocardiogram. MeRT uses the brain’s own redundancy of connections to reroute electrical signals through connections that still remain after injury or disease. Stimulating neurons with MeRT creates an electric current where there was a reduced signal. Like water taking the path of least resistance, electricity flows down the neuronal connections that still exist, creating new pathways where old ones were lost and strengthening weakened connections.

In this clinical trial by Taghva, et al., MeRT was used to treat Veterans with PTSD for 2 weeks. Results showed an average 42 % reduction in self-reported PTSD symptoms in every patient (n=16) that finished the trial. MeRT increased Alpha waves, which are seen in healthy controls and lacking in people with PTSD. Additionally these studies also show how MeRT increased Alpha waves in patients with traumatic brain injury (TBI), autism, major depression, and anxiety. Alpha waves are like pixels in the latest video game; the images are clear and transitions are smooth. However, these patients show a decrease in alpha waves. Their brains operate on a spectrum, depending on the severity, like the old Sega Genesis to the Atari; the picture and transitions are rough. For these people, only some aspects of their environment are picked up and encoded in the brain as a perception or only fragments of memories are recalled, if recalled at all. By stimulating the brain, new connections are made and existing connections become stronger to give function back; the Atari becomes an Xbox, and you become “you again”.

Can Mary Jane help your migraine?

By Cole Dawson, WSU Vancouver Neuroscience Student

From https://www.pinterest.com/pin/473089135829907716/

From https://www.pinterest.com/pin/473089135829907716/

Imagine the debilitating, sharp pain from a nail being driven through your skull. What kind of pain are you imagining? Can you imagine 3, 5, or even 10 more nails being hammered in? This is the exact pain migraine suffers feel, almost daily. Constant pain like this has a severely negative impact on day-to-day life. People see drops in production at work, get less enjoyment out of spending time with friends and family, everybody’s life becomes much more difficult to live. Migraine is the 2nd most disabling condition in the world and afflicts over 1/3 of the world’s population. Fortunately, there are treatments for migraines on the market, right? Well, these things often lead to what is called medication-overuse headache or MOH. MOH is characterized as a debilitating headache disorder caused by using anti-migraine therapies. So, the therapies on the market are causing headaches, which many people report as being worse than when they began treatment. This means that the current treatments for migraine lead to more migraines, that get even worse. Do we have treatments for migraine that don’t make headaches worse?

As many US citizens are aware, medical marijuana has been a very popular, yet controversial, topic over the past decade. Interest has been growing and news organizations are even dedicating feeds to keep everybody up to date on its status all over the US. Many news outlets provide success stories about medical marijuana stopping seizures, helping with chronic pain, and treating migraines. Despite the anecdotal success, there’s a significant lack scientific evidence to back up these stories.

Preclinical studies of migraine in rats is the first step to understanding how marijuana treats migraines. At this moment, the accepted model of assessing pain in a rodent is by measuring hypersensitivity. This is done by poking, prodding, or heating the injured area. This is odd, considering the clinical equivalence to this is heating or stabbing the site of pain. This is the last thing you need done when going to a physician, you just want to get rid of the pain! There is a more effective way for researchers to objectively assess pain, to get the most effective results that can translate into the clinical setting. This is done by measuring how often the rats run on a wheel.

Current research at Washington State University Vancouver tests the effectiveness of marijuana on migraines. More specifically, the main psychoactive component found in marijuana, known as THC. Work conducted by Dr. Michael Morgan at Washington State University Vancouver has shown that proper dosing and timing of THC can prevent a headache in an animal model, suggesting this may work in humans. These findings open the doors for THC as a migraine therapy. This helps propel the research of medical marijuana and gives the scientific community a foundation on the possible therapeutic effects of this drug.

Zika epidemic coming to a close?

By Sterling Gray, WSU Vancouver Neuroscience Student

The Zika epidemic could come to a close in the near future. A promising vaccine for Zika is moving into clinical trials shortly.

Zika is a virus transmitted by mosquitos that first appeared in Africa in 1947. From the 1960’s to the 1980’s the virus spread across South-east Asia and in the 2000’s made an appearance in the Americas. The United States, fortunately, has had a low contraction rate for the Zika virus. There have been around 5000 cases of Zika in the last couple years and the vast majority of them are contracted outside the States. The real problem lies within countries such as Brazil, where they’re reporting around 6500 cases every week.

Anyone can get Zika. For most people, Zika seems like the common cold characterized with a fever, sore throat, achy joints, and a possible rash. This doesn’t seem like a big issue right? The problem with Zika is it effects pregnant women the most profoundly. Not the pregnant women themselves, but their fetuses. Zika is linked to birth defects such as microcephaly (abnormally small head) and other neurological disorders in the last couple years, which is the reason it has been so attention grabbing.

So if this virus is so dangerous, why haven’t we developed a vaccine for it yet? Vaccines take some time to get through research and testing to make sure they are safe for the public, and many vaccines rely on a live-virus. This means they inject you with a weak form of the virus in order to give you a minor exposure, so your immune system can recognize it the next time you come in contact with it. Normally this is a safe method of vaccination, but in the case of Zika, even a minor exposure to this virus could potentially cause complications for a fetus. Recent research in a paper published in Nature has found a safe way to vaccinate without the risk of affecting the fetus.

Sterling pic1How does this vaccine work? Let’s use a person trying to infiltrate a building as an example. Let’s also say this building has security, but the security in this building only work their nine to five then go home to a wife and kids (bottom line they aren’t always at full attention Sterling pic2when there isn’t a threat). Now, what would happen if the intruder made an appearance and started causing havoc without any warning or way for the security guards to have even suspected an attack from this intruder? Well, the intruder would be able to infiltrate the building unnoticed and cause his havoc in the building. Eventually security would catch on to him, but even though security would be able to remove the intruder, the intruder would have already done the damage he set out to do. But! What if the security in the building had snap shots of the intruder’s face, what he is wearing, could track his cell phone and were expecting him BEFORE he attempted getting inside the building? Then if he tried to infiltrate the build, security would instantly recognize him and apprehend him before he had the chance of wreaking his havoc.

This is essentially how this vaccine works. The infiltrator is the Zika virus, the building is the body, and the information on the infiltrator is the vaccine. Without the information (vaccine), the infiltrator would be able to cause all the problems he had set out to do while your body’s security has a latent response to the disaster.

This new Zika vaccine is slightly different from other vaccines in that rather than giving someone a safe exposure to a virus, this vaccine carries information that allows your body to make the proteins Zika expresses. This allows your body to recognize Zika when it enters your body, devoid the risk of contracting Zika and adversely affecting the fetus of pregnant women.

So does this mean you shouldn’t be concerned about Zika? Well, not exactly. Since this vaccine is going into clinical trials, it may be another couple years or so until this vaccine reaches the public. Until then we will have load up on the bug spray.

When Lights Go Out, The Monsters Come Out

By Tanya Makarenko, WSU Vancouver Neuroscience Student

All of us, including me, have been afraid of the dark at one point in life. All of us, especially me, have been told there are no monsters hiding in the dark.  But people with epilepsy have good reason to be afraid, because there have monsters hiding in the dark. These monsters are seizures that are more likely to come occur at night.

Seizures are caused by abnormal brain activity. During a seizure, the brain cannot process the unorganized information it is receiving, like a smudged letter a person cannot understand. There are different types of seizures, a common one being a convulsive seizure. Convulsive seizures involve involuntary body movements.

The Official Journal of the International League Against Epilepsy, published a study looking at how melatonin affects the hippocampus. The hippocampus is a brain region that is involved in memory and emotions.  The study showed that convulsive seizures are correlated with melatonin. Melatonin is a hormone produced in your brain that controls your sleep patterns. Melatonin levels increase in the dark and decrease in the light. This explains why when it is dark outside, you have the urge to sleep and are awake during the day.

The study used rats to observe the effects of blocking melatonin receptors in hippocampal brain regions. A receptor (melatonin receptor) is like a lock and the molecule that binds to the receptor (melatonin hormone) is like the key. Once the key opens the lock, the door opens allowing a chain of events to proceed. They used molecules to block the melatonin receptors. The rats were observed in the day and night through behavioral activity, EEG (machine recording brain waves) and seizure susceptibility.

One of their most profound discoveries was that in the dark phase (night) melatonin levels rose, and blocked GABA receptors, increasing the probability of seizure occurrence. GABA molecules inhibit brain activity. By blocking this protection, the chances of seizures increases.

The information discovered by this study is ground breaking, the molecule allowing us to sleep opens the door to monsters (seizures) in epilepsy patients. We do not know why melatonin acts differently in the night vs day. It is up to future studies to tackle the information gathered in this study and use it to find an explanation.

THC and Opioids: The Future for Pain Management?

By Alexander Tran, WSU Vancouver Neuroscience Student

Alex figure1“Ouch!” Probably one of the most common words you’ll hear as a parent. Pain is an unavoidable sensation and it is protective to our bodies. We experience pain almost every day and for the most part it isn’t a distraction to our lives. But what happens when we have surgery and the next day and our son wants to play catch the next day? It hurts to breathe let alone stand up and I’m expected to play catch? What if you had to work the next day to feed your family? Well, the doctor probably gave you some pills to help you manage your pain, so take some and let’s go play catch! You pop your pills and as soon as you stand up nausea and dizziness overwhelm you and you’re back on your back. How can a doctor prescribe me a pill that is supposed to make me feel better but made me feel even worse? Why am I constipated? What did I just take? Opioids are probably the culprit for these sensations. Unfortunately, although the pain is gone, the side effects are unavoidable.

Alex figure2Fortunately for us, there may be a better way. Researchers at the University of Texas Health Science Center are researching the potential of cannabis (tetrahydrocannabinol, THC) in treating pain. Now you may be thinking something along the lines of… “WHAT?” You may also be thinking that I’m crazy and you’re probably also moving your mouse to the X at the top of the screen. THC may have a bad rap because of the way it is used, the people typically using it and the negative stigma attached to it but this drug has the potential to let you lay down on your bed after a surgery and relax without discomfort caused by opioids. Would you prefer to relax in bed or would you prefer to relax beside the toilet?

Tetrahydrocannabinol (THC) is the main constituent of cannabis a.k.a. marijuana. It is classified by the DEA as a schedule I drug, the highest classification for potentially dangerous drugs. For this sole reason, we can see why there is so much concern over THC. Do I have to roll a blunt for my kid after a wisdom tooth extraction? Maybe I have to make him a special brownie milkshake? Will my child get addicted to marijuana? There is a lot to THC that we do not know but what we do know is that THC is safe and easy to use, provides pain relief and has a synthetic form that is prescribed to civilians under the name dronabinol. And no, you don’t have to cook it into a brownie.

Alex figure3David R. Maguire and Charles P. France are scientists at the University of Texas who are investigating the potential of THC in treating people suffering from pain. Previous research showcased that the use of both THC and opioids, drugs (Vicodin, morphine, etc.) that are commonly prescribed for pain management, increased the strength of opioids without the side effects that are commonly associated with opioid use. Maguire and France used this research and performed their own research on rhesus monkeys to find the opioid that THC best pairs with. They gave the monkeys commonly prescribed opioids of different strengths; morphine, fentanyl, etorphine, buprenorphrine and nalbuphine, in conjunction with THC and examined the effects of THC on the strength of these opioids. They found that depending on the strength of the opioid, THC had different effects. The stronger the opioid, the stronger of an effect it has when THC is taken with it. For example, fentanyl, one of the strongest opioids, was stronger by over 20 times (upwards to 50 times stronger) while, morphine, a weaker opioid, was only stronger by was only stronger by approximately 5 times when used with THC. THC then has a lot of potential in the medical field and can help millions of people.

So sure, THC can help millions of people and can make the pain go away but do I still have to have my son smoke a blunt? The answer to this question is, no. THC can be a glassy solid that can be mixed into a typical opioid pill, so when you take it, you won’t even know you took it unless the doctor told you. What is important to note is that patients will not have easy access to THC nor will they be given only THC unless they purchase it legally from a provider. Additionally, the amount of THC needed is minimal so any risks associated with THC use are minimal at best. This research shows that THC has therapeutic properties and medical potential that can be utilized to improve an already established treatment for chronic pain.

 Would you like some more? The Science Behind Binge Eating

By Samuel VanCleef, WSU Vancouver Neuroscience Student

Sam graphic1Why is it when your stomach is still screaming “feed me Seymour!”(like in the Little Shop of Horrors) and you have already unwillingly and unknowingly eaten twice the amount you wanted? This behavior is referred to as binge eating and can potentially lead to binge eating disorder.

Binge eating is the process of uncontrollably eating large amounts of food in a short period of time. This, however, is a perfectly normal behavior which effects everyone including the author of this paper who has a particular weakness for Swedish Fish. When a person’s binge eating habits become more frequent in a week or a day this person might be categorized as having a binge eating disorder. According to the National Eating Disorder Association, binge eating affects 3.5% of women and 2% of men. Although binge eating disorder is the most common eating disorder, it remains understudied and the impact it has on our brains is not yet understood.

Although the neurological effects of binge eating are not yet understood a study performed by Karen Smith’s lab in Boston is looking at a potential contributor to the mechanism of binge eating. Karen Smith theorized that the main contributor of binge eating went through N-methyl-D-Aspartate (NMDA) receptors. These NMDA receptors contribute to neurons being strengthened or weakened over time allowing for stronger or weaker impulses or behaviors. Receptors act like locked doors that can only be opened with specific types of keys which are molecules. To test if these receptors participate in binge eating, experimenters took two groups of mice, on group of mice received normal Chow while the other group received high sugar Chow. The Chow food contained all of the nutrients that the mice needed to grow up healthy and strong, but the sugary Chow tasted like chocolate. It was like choosing between having a chocolate donut or a roll of bread. The experimenters then determined the overall Chow intake that both of the groups of mice ate. The two groups were then injected with a NMDA receptor blocker, preventing these receptors from being activated. When injected, the normal eating behavior mice showed no difference in their eating behaviors while the binge eating group showed a remarkable difference. These binge eating mice showed a reduction in their binge eating behavior. This reduced binge eating behavior which resembled the normal group of mice that received the Chow.

Sam graphic2

What this test shows is that NMDA receptors play a contributing role in binge eating. This finding not only reveals that NMDA can cause binge eating to occur but suggest a potential treatment for this disorder. Treatment of binge eating disorder could follow this research to block either the NMDA receptors themselves or even downstream targets that the NMDA receptors effect. However, further studies should look into this mechanism that binge eating inflicts. This could help answer questions about why people unknowingly and compulsively eat large amount of food.

Sam graphic3






 New Hope for Multiple Sclerosis Sufferers

By Anna Pearson, WSU Vancouver Neuroscience Student

Take a moment out of your hectic life to watch the orange sunset, whether it’s watching it on the deck of your beach house or on top of a mountain. In fact, the beautiful sunset is most rewarding after trekking up the mountainside, placing one foot in front of the other for miles on end. The view and crisp mountain air is invigorating and inspiring after a long hike.

Now imagine a time where you can’t actually make the journey up the mountain to that alluring sunset. You’re now in a situation where you lack control of your own body and you can’t walk in your own home, let alone up a rocky incline. You may possess the drive to make that climb, but it’s your body that’s preventing your thoughts from becoming actions. In a cruel reality, you’re trapped within your own body.

Anna-graphicThat’s what it’s like for sufferers of multiple sclerosis, or MS. Multiple sclerosis is an autoimmune disease that wreaks havoc on the lives of 2.5 million people worldwide, inflicting serious disabilities as it strikes the various parts of the body. People endure difficulties with coordination, balance, vision, and movement, where their hands tremble, speech is slurred, and eyesight fails. These impairments are due to the loss of the myelin sheath, the protective coating around cells that expedites communication between the cells in the body and enables us to move around freely. In MS, the myelin sheath is lost when the body begins to attack and destroy its own brain cells. While poorly understood, inflammation in the nervous system contributes to the degeneration of the brain cells, thus exacerbating the progression of the disease.

Unfortunately, there is still no cure for MS and current treatments are widely ineffective. In an attempt to relieve MS sufferers and develop preventative care, Dr. Tadhg Crowley of University College Cork in Ireland and his colleagues study inflammation associated with MS. Their current focus is the relationship between baclofen, a muscle relaxer, and inflammation in the brain in relapsing-remitting MS patients. Most people with MS suffer from the relapsing-remitting form, where individuals experience intense flares of symptoms followed by times of remission. In most cases, this relapsing-remitting form develops into a progressive form, where symptoms continuously worsen over time.

Baclofen is already prescribed to those experiencing muscle tightness as it acts on GABA receptors. These receptors are known to have an inhibitory effect, where they work as small machines that signal a process to come to a halt, like a stop sign to disengage your muscles. GABA receptors have been found on the cells that encourage inflammation, making them an interest to scientists. Crowley and his associates speculate that baclofen could be used to stop inflammation by activating these inhibitory GABA receptors to stop the creation of cells that cause inflammation. In simple terms, the scientists wanted to see if baclofen could halt brain cell degeneration and improve MS symptoms by turning on these GABA receptors.

The Irish scientists discovered that baclofen reduced the amount of cells that cause inflammation in healthy cells. This suggests baclofen may offer better preventative care than treatment. However baclofen hindered the synthesis of pro-inflammatory agents in immune cells, indicating anti-inflammatory properties. Most importantly, the research strengthened a link between GABA receptors and brain diseases as less of these receptors were seen in relapsing-remitting MS patients, proposing GABA receptors mediate the body’s attacks on itself.

Expansion of these findings by Crowley and his collaborators help improve understanding of how neural inflammation contributes to brain cell damage and dysfunction in people. By enhancing the bigger picture of how neural inflammation affects the body, treatments can better target underlying causes and restore mental and physical abilities. These understandings can even be translated into other diseases, such as Parkinson’s or Alzheimer’s disease, that share similar inflammatory qualities. Scientists continue to identify therapies that revamp prognosis and restore hope. One day, people will be able to say they used to have multiple sclerosis as they climb back up the mountaintop to witness the sun pass the horizon.

Turn Down for What? … To Save Your Hearing!

By Beija Villalpando, WSU Vancouver Neuroscience Student

What do blow dryers, rock concerts, and heavy road traffic all have in common? All three produce noise loud enough to cause permanent hearing loss, a problem affecting over 10 million Americans! While there is a common misconception that hearing loss primarily effects elderly populations, people of all ages are susceptible, with excessive noise exposure being the major culprit of hearing loss.

To understand noise induced hearing loss, we need to understand how we hear. Humans are able to detect sound using specialized cells located deep within our inner ears, called hair cells. Appropriately named, hair cells contain hair-like projections that dance from side to side when stimulated by sounds entering the ear. When exposed to excessive noise, hair cells are damaged, eventually die, and cannot be re-grown, which results in permanent hearing loss.



The Occupational Safety and Health Administration (OSHA) reports that hearing loss can be caused by sounds of 85 decibels, which is comparable to the sound of heavy traffic. If such common noises cause hearing loss, what methods are available to help us protect our hearing? Currently, only one method exists, earplugs – but how do we protect our hair cells when loud noises are unexpected, when loud noises overcome the protection of earplugs, or when we don’t have our earplugs handy?

To answer these questions, I study zebrafish in the Coffin Lab at WSU Vancouver. These eyelash-sized fish have hair cells located on the sides of their body that are similar to the hair cells found in human inner ears. Unlike humans, zebrafish are able to regenerate their damaged hair cells! However, just like humans, zebrafish exhibit duration dependent hair cell death: put simply, the longer they are exposed to excessive noise, the greater their hair cell death. Additionally, my research shows that humans and zebrafish share similar mechanisms for noise-induced hair cell death, including death by radical oxygen species (ROS), also known as free radicals. Zebrafish hair cells can be protected from ROS damage using antioxidants, molecules found in blueberries, green tea, and dark chocolate. Clinical trials testing the efficacy of antioxidants to protect hair cells from noise damage in humans have shown inconclusive results, indicating the need for discovery of additional therapeutic treatments. Using noise-exposed zebrafish, I plan on testing approximately five hundred drugs found in nature that may protect against noise damage. Once identified, these drugs will hopefully prevent noise-induced hearing loss in humans!

In the mean time, I’ll leave you with a few tips to protect your hair cells. First, many people turn up their headphones’ volume to block out other noises, but don’t! Instead, set your headphones’ volume in a quiet environment, and try using noise-cancelling headphones so you can keep the volume low. Secondly, be aware of common dangerous noise levels, so you know what sounds are damaging to your hair cells. Finally, keep a pair of earplugs handy, because currently, earplugs are the only protection your hair cells have!

 Can we learn to work while we sleep?

By Arthur Serkov, WSU Vancouver Neuroscience Student

SerkovIn 2010 the popular Christopher Nolan film Inception staring Leonardo DiCaprio and Joseph Gordon-Levitt was released. The recurring theme of the film was entering another person’s mind during their sleep and somehow extracting important secrets and doing lots of cool stunts. While a lot of the movie was just Hollywood being Hollywood, it was inspired by an actual practice known as lucid dreaming. Lucid dreaming is what happens when a person is able to keep their conscious mind awake while they are sleeping. Recent research by German scientists has helped understand more about the mechanisms that allow some people to be in full control of their dreams. This practice has been gaining popularity lately, and for some, has helped to have more control over their lives. The claimed benefits range from helping overcome relationship problems, all the way to solving the deeper questions in life, simply because practitioners have more time at night to process it all. So can anybody lucid dream, and if so, how does one start? That is the exact question that I asked myself before I embarked on my quest to be productive even during my sleep.

Going into a lucid dream involves doing a reality check during the day, keeping a dream journal, and trying your best to meditate on being conscious as you fall asleep. These were all the steps that I began to follow, yet for some reason while trying to achieve this state, I ended up not sleeping well for about a week before giving up. What was the problem? I started to look into why some people seemingly can dream lucidly with ease, while others like myself had to struggle so much with it. That’s where recent research into this subject comes in. German scientists did a study of two groups of people, one that dreamt lucidly often, and one that didn’t dream lucidly at all. They had the participants brains scanned by a powerful magnetic machine called an fMRI and monitored the activities in their brains while they performed lucid-like activities. What they found was that there was activation in a small area at the front of the brain during these tasks. Interestingly, the highly lucid group had a lot more brain cells in that area, known as Brodman’s area 9, to begin with. This is the area right behind the top of your forehead and is important for things such as short term memory, error detection, and processing emotional questions. This essentially means that the reason the people in the study can detect discrepancies in their dreams, and have memory of the dreams is because that area of the brain has a lot more cells than in an average brain, and certainly more than in my brain.

Upon reading that paper I began to wonder if I was one of those people with a normal brain, or worse yet, what if I was someone with even less brain cells in that area than normal? I then realized that for most things in life there were those people who were naturally good at things, and then the rest of us who had to get what we wanted through hard work and dedication. Sure enough, looking over the forums, some people spent a month, some up to 3 months, but just about everyone was able to achieve the ability to lucid dream. So now that research has illuminated why some of us are not able to lucid dream as easily, it just remains to figure out how to make us all “work” as we dream.

 A Handy Prediction: Carpal Tunnel Surgery

By Levi van Tol, WSU Vancouver Neuroscience Student

How would you feel to walk into a dark room and search the wall for a light switch but a numbness in your hands prevents you from finding that switch? What if you were at a restaurant with friends and pick up your glass but it shatters against the floor because you can’t keep your grip on it and everyone stares? Or maybe you need to type an email to a co-worker but you can’t get those thoughts on the screen because you can’t feel the keys. These are just a few scenarios that people with carpal tunnel syndrome face every day. Carpal tunnel syndrome is diagnosed in the United States about 3 million times per year. Most people know someone affected by carpal tunnel syndrome; for me, my father has had carpal tunnel syndrome in both of hands. The pain often kept him up at night and his hand use was greatly impaired from the numbing sensations. He told me about the problems he had trying to perform at work and play baseball with me as a child. The frustration he felt in not being able to participate was apparent. Carpal tunnel syndrome occurs because of some breakdown or inflammation in the area of the wrist and palm. At the base of the palm side of the hand, underneath the skin, the carpal tunnel is the route all of our nerves and tendons take to reach our fingers. Nerves relay information from the brain to tell muscles when to contract for instance. Tendons attach from muscles to bones and are vital to the proper movement of the hand in this case. When the nerves and tendons are under pressure, the hand feels numb and the proper range of motion for the fingers is decreased. Carpal tunnel is very treatable through surgery like the kind my father had on his hands. Surgery can be open or endoscopic. Open surgery uses a large incision on the palm while endoscopic surgery uses two small incisions and a camera. Surgery cuts through the carpal ligament which is a sheet of tissue that can often release the pressure on the carpal tunnel once it’s removed. Once the surgery is performed most patients feel fully restored and they relay this information to their doctors. But when I asked my father if he was ever tested to see how effective the surgery was from an objective standpoint he said no. The term objective refers to, in this case, a standpoint that is already set without the opinion of the patient.

With this information in mind I set sail on testing the surgery’s effectiveness because who knows, it might not even work from an objective stand point. Using patients who all had carpal tunnel surgery in the past 10 years, I measured the grip strength, pinch strength, and manual dexterity of 42 hands. Grip strength and pinch strength are measurements that determine how strong certain hand and finger positions are. Manual dexterity refers to a person’s ability to grab and move objects. With this data I was able to compare scores of former carpal tunnel syndrome patients to healthy individuals that didn’t have carpal tunnel syndrome. For the strength and dexterity measurements, normal meant that the patients didn’t have any ailments that could affect their hand function. The normative data is also compiled by sex and age for the most accurate comparisons. My findings show that carpal tunnel surgery is fully effective long term. In the context of my dad, he was not only able to get right back to his activities like playing baseball with me, but also can with his grandkids now and into the years to come.

These findings are significant because surgeons and doctors can now give accurate predictions about future outcomes to patients who need carpal tunnel release. Also, the elderly population in the United States is growing and the need for effective carpal tunnel release is absolutely necessary for the proper use of assistive walking devices. Assistive devices like walkers are vital in preventing falls for the elderly. If the hand is being affected by carpal tunnel syndrome, the numbness could cause an accident in handling the assistive device. Often a fall can lead to hip fracture which greatly disable the mobility and independence for the person. I would like to further this research with a greater sample size. In addition, it would be interesting to look at effectiveness differences between open carpal tunnel release and endoscopic tunnel release so that doctors could refer patients to surgeons who perform one type of surgery or the other. If you or someone you know needs carpal tunnel surgery, the outcome is very positive and now that isn’t just a matter of opinion.


Musical Rats: Analyzing Ultrasonic Vocalizations to Understand Rat Behavior

By Priya Kudva, WSU Vancouver Neuroscience Student

Priya-graphicWhat if I told you that every single one of the 7.4 billion people will be or already is addicted to something? This includes you. You may not be addicted to drugs, but you could be addicted to something as simple as chocolate or Facebook. Either way, being addicted can be scary.

Officially classified as a mental disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), addiction can be split into two types: substance use and behavioral. As a researcher and student, I study the mechanisms and behaviors of substance-addicted rats, and admittedly, it is much easier to get a rat addicted to cocaine than to Facebook.

However, this intrigued me. How can we truly measure the behavioral aspects of an addicted rat? One way that most researchers have measured behavior is through a procedure called Conditioned-Place Preference (CPP). In CPP, rats are placed into a box that has 2 distinct compartments, distinguished through their different flooring and wall patterns, which we can simplify to just the white and black side. The rats are trained to associate one side with a drug (positive) and the other side with saline (neutral). After training, the rats should prefer to be in the compartment that they got drug in, much like you would prefer a room with toys rather than an empty room. What the researchers measure is how much time they spend in that compartment versus the other. Even though this is one of the most used methods for measuring a rat’s behavior, when we want to translate this to a human’s behavior, we have to consider some other factors.

One of these factors is that there can be some differences in communication. Though rats are a social species and they can communicate with each other, we can’t understand what they are saying. We can’t tell if they went to the black side of the box because they got cocaine or because they don’t like the white side. To hopefully crack the “rat communication code”, I analyze their calls, otherwise known as Ultrasonic Vocalizations (USVs) because they are in the ultrasonic sound range. After analyzing dozens of recordings, I have developed a key to some of the USVs we see rats exhibit. I have found that rats call at a higher pitch when they received something positive (like cocaine), much like our voice volume can increase when we are happy or excited. At the same time, rats call at a lower pitch when they experience something negative (like a shock), much like our voice volume can decrease when we are scared or sad.

With this research, we can provide a separate method and key of analyzing behavior in rats that can help provide more answers for what drugs do to not only our body but also our psyche. Patrick J. Kennedy once quoted, “No one is immune to addiction; it afflicts people of all ages, races, classes, and professions.” So what are you addicted to?


Protein Clumps Linked to Alzheimer’s Disease Are Found in People with Head Injuries

By Diana Latypova, WSU Vancouver Neuroscience Student

Diana graphicIf you have ever experienced a severe head injury, you are at an increased risk of developing Alzheimer’s disease, a form of dementia, later on in life. Scientists from Imperial College London are now able to show the long-term relationship between Alzheimer’s disease and head injuries.

A hallmark characteristic of the progression of Alzheimer’s disease is the accumulation of harmful protein clumps in the brain. These clumps are made up of one specific protein that becomes clumped together. The presence of these clumps works like a plugged toilet except in the brain. When too many protein clumps build up, they impede the flow of toxic waste from the brain and block essential cellular functions. Eventually, this blockage causes the death of brain cells. People who have had a head injury also show the presence of these clumps.

The scientists from Imperial College London looked at the presence of the protein clumps in nine, middle aged individuals. The range of when the head injuries were obtained ranged from 11 months to 17 years prior to the study. The scientists took brain scans that allowed them to visualize the protein clumps. Scans were viewed from the individuals who had sustained a head injury. Scans were also viewed from healthy individuals and individuals with Alzheimer’s.

The team found that the individuals who had sustained a head injury had more protein clumps than healthy individuals, but not as much as the individuals with Alzheimer’s. The clumps were found in two specific areas of the brain: an area that is responsible for attention and memory and an area responsible for controlling and coordinating body movements.

In addition to looking at the protein clumps, the team also looked to see if there was damage to the wires of the brain which connect brain cells. This wiring is important for communication between brain cells because it functions like a circuit board that connects all of the important pieces. The scientists found damage to the wiring in the same brain structures where the protein clumps were found.

These results show that the effects of a head injury still persist many years afterwards. This study also shows that there may be a relationship between damage to the brains wiring and the creation of harmful protein clumps. The next step is to figure out the biological process of protein clump formation and hopefully develop better treatments for individuals with head injuries. So, the next time you decide to participate in a high contact sport, be sure to wear a helmet or other protective gear for your noggin.

 Women, Migraines and Marijuana

By Courtney Miskell, WSU Vancouver Neuroscience Student

Everyone knows the horrible feeling of stubbing their little toe on their bed frame first thing in the morning. We can recall the consequent throbbing, holding your foot while in the fetal position and however illogical, promising to destructively burn your furniture. Now imagine waking up and repeatedly kicking your bed frame; I don’t enjoy the feeling of constant throbbing pain but is what I experience suffering from chronic migraines.



Rather than my little toe, the throbbing is the left side of my head and it comes with a wealth of debilitating factors such as nausea, vomiting, sensitivity to light, sounds and smells. During an episode migraine sufferers, myself included, are unable to maintain their normal daily routine and often miss work, school and social functions. It is estimated that in a given year American employers lose more than $13 billion as a result of 113 million missed workdays due to migraines.

Migraines are the eight most disabling illness in the World and an estimated 70% of sufferers are women. While I’d like to know why women suffer more frequently from a migraine I’m particularly interested in ridding the pain and finding a more effective treatment. This is because sufferers who take medication for each episode experience a phenomenon called medication overuse headache, or MOH as researchers call it. The MOH condition says that repeatedly using medication to alleviate migraine pain, prescribed or over the counter, actually worsen the chronic illness. In all its sadist glory the episodes are longer, more frequent and more painful for the sufferer.

Although females are disproportionately affected, many migraine research studies to find more effective treatment and better understand the illness have used only male rodents. Additionally the common way to assess pain has been using hypersensitivity tests. The human equivalent would be seeing a doctor and having them repeatedly hit you in the forehead to determine whether or not you have a migraine. As we know and have hopefully never experienced, this is not diagnosing criteria. Instead, the criteria is the lack of activity and behavior associated to the pain. My research with female rats aims to assess migraine pain similarly. While my rats can’t verbally tell me how they feel I can observe their behavior before and after a migraine and thus, determine the effectiveness of their treatment.

We’ve learned that repeated use of common medications doesn’t improve the condition. This is why I am using THC, a component of marijuana, as the treatment. As the legal constraints decline, self reported use of marijuana for migraine pain increases. While THC’s ability to reduce pain has been reported globally, similar research conditions have not been assessed in a rodent model. I am hopeful that my research can offer insight for a more effective treatment option that may help the many sufferers that are unable to experience relief without a trade off such as MOH and continue to be confined to the unfavorable impacts of migraines. The call for cannabinoid research is loud and the anecdotal evidence of use for chronic pain is indisputable meaning THC may be the golden ticket for sufferers of chronic migraine pain.

 Listen up! Using mice to make some sense of human speech processing

By Mickey Dunn, WSU Vancouver Neuroscience Student

Imagine a typical encounter with a person in your life. This could be your significant other, your classmate, or even a coworker. They might be asking you what you want for breakfast, what chapter to read for Tuesday, or which room the meeting will be held in at 3 o’clock. Although these social situations are all pretty different, they all involve one of the most mysterious functions of your brain.

Sound processing can be loosely defined as your brain’s ability to receive, identify, and make decisions based on the sounds around you. Despite listening seeming like a straightforward task, for a person with Central Auditory Processing Disorder (CAPD), it can be a complete nightmare. CAPD is the inability of a person to make sense of what’s been said to them even if their hearing is completely normal.

The way the brain seems to be “messing up” is not totally understood largely because the way the brain is processing sound normally is not totally understood, either.

In the lab of Dr. Christine Portfors at Washington State University Vancouver, we are figuring out what the brain is actually doing when its listening to socially relevant sounds. The mouse brain, which has most of the same “listening” parts as a human brain, is responsible for doing what ours does in terms of sound processing. Mice emit ultrasonic vocalizations (USVs) in social situations. Males may vocalize in an attempt to woo a female, and mouse pups often emit USVs to attract the attention of their mother. These sounds range in complexity and are being studied for their variability; some scientists even claim that these vocalizations are context-specific, meaning mice change what they say based on to whom they say it. For these reasons, mouse vocalizations are sometimes compared to speech. Also like humans, mice need to be able to receive, process, and make decisions based on the sounds around them.

The portion of mouse sound processing that I’m interested in is the identification part. How are mice specifically (and mammals in general) able to determine what a sound means?

By using electrophysiology, I can record how the mouse responds to sounds I present to it. I put an electrode into a part of the brain responsible for processing sound and play USVs to the mouse to change brain activity. If the brain cell I’ve isolated likes the sound, brain activity changes. If the brain cell doesn’t like the sound, nothing changes. By taking note of the way single cells responds to different types of vocalizations, I can make predictions about the way the brain is interpreting sound.

Below is an Instagram photo I snapped while analyzing data.  The colorful spikes are action potentials (the electrical signals brain cells use to communicate with one another) that were firing in response to the sound stimulus I was presenting. Data is best when rainbow.

Mickey graphicAlthough the way mice and humans are listening to socially relevant sounds isn’t entirely clear yet, we’re getting closer to understanding why different vocalizations can evoke different responses in the mouse. Once we’ve established a baseline of what normal responses look like, we can start using mouse models of communication disorders like CAPD to find out why sound processing sometimes goes awry. In the meantime, I and my colleagues, among many others around the world, are racing to uncover how the most complicated part of the body is doing one of the most important and most puzzling functions. Understanding human speech is no longer just about listening; we’re learning that it involves precise networking between brain cells to let us perform one of the most rewarding tasks. Imagine never having understood any of the words that have ever been said to you; none of the questions, affectionate affirmations, or scoldings would have any emotional significance. Now imagine, for the first time, making sense of what’s being said to you. This moment is what scientists are striving to give to people with disorders like CAPD, and we’re closer than ever to accomplishing that.

 Run for your life!

By Hanna Morris-Pinson, WSU Vancouver Neuroscience Student

Exercise, running, and sweating…. At first thought, you might cringe at these three words. However, you might change your mind if you knew some of the positive benefits. No, I’m not talking about increased endurance, weight loss, or endorphins. I’m talking about a potential to delay or reverse the side effects of neurodegenerative diseases like Alzheimer’s disease (AD). Alzheimer’s disease is characterized by the buildup of a plaque-like substance, amyloid-beta, resulting in decreased cognitive abilities caused by shrinkage of the brain. The reduction of neuronal brain connections seen in AD patients leads to difficulties recalling and making new memories. AD is most associated with the hippocampus, a portion of the brain responsible for learning and memory. Currently, there is no known cure for AD, and there is still much to be understood about the progression of the disease.

Hanna-picA recent study published in Neurobiology of Learning and Memory utilized genetically modified mice to analyze the effects running had on the progression of AD. The mice laced up their running shoes and ran for AD. Control non-AD mice simply ran for ten minutes a day, but AD mice ran, ran, and ran until their shoes wore out. Okay, not really, but image seeing a mouse wearing running shoes while running a 5k on a treadmill!

Results found that running may be associated with activating the brain derived neurotrophic factor (BDNF) process, a process that promotes the protections of neurons and neuroplasticity. Neuroplasticity is the brain’s ability to essentially rewire/tune itself, to adjust to the environment. The BDNF process, upon exercise, was found to significantly decrease the amount of amyloid beta build up in the brain, and promote neuroplasticity and the protection of neurons. This finding could be monumental in understanding AD! As we know, the symptoms of AD are due to the over accumulation of amyloid beta in the brain. Many use to believe that in AD patients, amyloid beta over accumulated because the brain was overproducing it, but this finding suggests the opposite! This finding suggests that the brain of AD patients aren’t making too much of the buildup, it’s actually making the same amount, but the brain is under producing a substance that clears the plaque-like buildup from the brain. You could think of this like going to the supermarket on a day in which they were short on staff, and it took you forever to check out, not because the checkers were slow, but because there just aren’t enough on staff for the demand of people in the store! That’s the worst. Well, that’s like what’s going on in the brain of individual’s with AD, they don’t have enough checkers to clear away the buildup. Upon exercise though, the buildup in the brain significantly decreases because it helps activate substances that clear them away. Or, in terms of the supermarket, they properly scheduled their employees so customers could quickly get through the line and continue with their day.

Additionally, the study found that early damage of AD could be seen first in amygdala, a portion of the brain associated with memory and emotions, rather than the hippocampus. This finding is surprising as many only associate AD with the hippocampus, and not the amygdala, because of the learning and memory impairment of AD! However, this helps us understand why people with AD often have difficulty recalling memories!

This is pretty exciting news and means that we are one step closer to better understanding the components that lead to the disease! As much as I’m sure you may want to hate running because it can be both physically challenging and exhausting, it poses for a wonderful therapeutic approach to curing AD. You can’t deny that this is amazing and could lead to such great advances regarding the quality of life of individuals with AD. These new findings help us better understand the progression of the AD and how exercise may be used to delay and even reverse the neurodegenerative effects of AD through activating a route responsible for protecting the brains connections. So, perhaps now you may want to hit the pavement running!

 The Importance of Sugarcoating Neurons

By Kelsey O’Neill, WSU Vancouver Neuroscience Student

Have you ever wondered how you can walk down the street, looking at your phone, and manage to fairly seamlessly weave through the crowd? Most of the time, we manage not to run into any obstacles in our way, such as a pole, because we are able to recognize the new things in our environment and respond. This is an important survival mechanism, as we need to know when threats appear in our environment so we can adapt and respond. This ability to notice change in our environment is called recognition memory.

Simons & Spiers 2003

Simons & Spiers 2003

Recognition memory is housed in a specific region of the brain known as the medial prefrontal cortex, the part shown in light purple in the image on the right.

The medial prefrontal cortex, like all other brain areas, consists of specialized cells called neurons. When you think of brain cells, you probably think of neurons. But the nets that surround these neurons probably do not come to mind. These are called perineuronal nets or PNNs.

Geissler et al. 2013

Geissler et al. 2013

What are these perineuronal nets? The prefix “peri” means around and “neuronal” means neuron, so these are literally nets that surround neurons or PNNs. The PNNs are made up of sugars and proteins that form a sort of meshwork around neurons. PNNs are much less studied than their neuron counterparts but may play a much larger role than just support and structure for neurons. PNNs can also be broken down using an enzyme that acts like a Pac-man and chews them up.

The goal of my research as a member of Dr. Barbara Sorg’s Neuroscience lab at WSUV was to investigate how breaking down the PNNs in the medial prefrontal cortex impacts recognition memory. In order to test recognition memory, we exposed rats to objects that they had seen before and objects that they had not seen before. So though bottles and Legos may not seem exciting to you, they are new and exciting to rats. Or they should be if their recognition memory is functioning properly. The findings of my study were that when the PNNs were chewed up in the medial prefrontal cortex, the rats failed to recognize the novel object in their environment and thus exhibited short-term impairment of recognition memory.

Why does that matter? As mentioned earlier, PNNs have had very little stage time in terms of research history. Italian biologist Camillo Golgi first described the unique, lattice-like structures surrounding neurons in 1898. Unfortunately, many assumed they were a product of improper staining technique by Golgi and thus disregarded these nets. It was long believed that PNNs provide the structure while the neurons do all of the heavy lifting in terms of cognitive function. My study shows that the loss of PNNs in a very small area of the brain impairs a very specialized form of memory. This defies the beliefs held for half a century and proves that PNNs are essential for specialized cognitive processes. My study demonstrates that PNNs are worth studying and provides promising potential for future research in PNNs due to their pivotal role in recognition memory. In conclusion, your ability to recognize when someone enters your path on the street hinges upon the intricate nets surrounding neurons, thus demonstrating the importance of sugarcoating neurons.

 Well, I just blue myself

By Nathan Allen, WSU Vancouver Neuroscience Student

You have just suffered the worst spinal injury of your life after being smashed up against a divider on what was supposed to be a joyride on your new motorcycle. You cannot move, but you can faintly hear the ambulance coming, the sirens getting louder. Paramedics approach and give you an injection near your spine. Bordering on the edge of consciousness, you think you may make a recovery with their quick help… and then you notice your skin begins to turn a hint of blue. “It’s a part of the process,” says the paramedic “don’t worry about the color.”



It’s all in a day’s work of Brilliant Blue G (BBG), a food grade dye that researchers have discovered has incredible medical benefit. The dye is already used in things such as ice creams, candy, and blue raspberry flavored products. Researchers began to test the dye for its medicinal properties when they noticed that its chemical structure was similar to many anti-inflammatory drugs. They found that BBG reduced the inflammatory response in rats with spinal injuries, and in those same rats, BBG also caused a quicker recovery period when compared to rats who received no BBG. The only noticeable detriment to the rats was a bluish hue that their skin took on after administration of the dye; a hue which caused no adverse effects and was completely gone in a week. Granted, the motorcycle scenario above is a far stretch from the current reality of BBG, but the therapeutic potential exists. It crosses the blood-brain barrier, the human body’s natural filter that prevents harmful substances from entering the blood of the brain and spinal cord, and appears to be non-toxic.

What’s more, recent research has shown that BBG is effective in treating the mental and spatial memory damage seen in Alzheimer’s Disease. Researchers subjected mice who were injected with a protein called amyloid beta (basically the mice equivalent of Alzheimer’s Disease) to a water maze task and a novel object recognition task which track mental and spatial awareness. The water maze causes mice to swim to an elevated platform located randomly in the maze while the novel object recognition task tracks exploratory time of the mice with certain objects. These tasks are a common way among mice and rats to test their memory, analogous to Grandma finding her favorite supermarket in town, or remembering that her favorite grandson is red-haired, short, and named Jimmy. Compared to their non-Alzheimer’s disease mice friends, mice injected with BBG had very similar “escape latency” times for the water maze; basically, how long it took them to escape or find the elevated platform so they could stop swimming. Alzheimer’s Disease expressing mice who did not receive the BBG injection performed worse on all tasks.

After seeing the positive benefits of these BBG injections, the same researchers took hippocampal cells from mice, grew them in a dish, and injected them again with amyloid beta. The hippocampal region, and thus its cells, are responsible for a great deal of memory retention and in those with Alzheimer’s Disease, brain cells in the hippocampal region have a drastically reduced number of dendritic spines. Dendritic spines are little nodes on brain cells that allow other brain cells to latch onto them and communicate, sort of enabling a crosstalk channel. These same researchers found that injecting BBG after amyloid beta into these hippocampal neurons recovered the loss of dendritic spines when compared to hippocampal cells that just got the amyloid beta injection.

So, a food grade dye that has great therapeutic benefit, so what? Well, to researchers who are looking for a persistent and effective treatment against Alzheimer’s Disease, which effects more than 5 million seniors today, BBG may just be what is needed. Additionally, since the spinal cord is essentially the shield of all your limb’s nerve input and output, any damage to it is extremely debilitating. A molecule or drug that is an anti-inflammatory, speeds up motor recovery, and has the ability to
cross the blood brain barrier is huge, as the development of many beneficial drugs has been halted due to their inability to cross this selective blockade. And not only can it cross the blood brain barrier, but it’s non-toxic to boot.

So here’s to hoping that years into the future, “smurfing” will be a commonplace word:
Smurfing (verb): To rapidly heal from spinal cord injury, denoted by the skin’s temporary blue color.


Treating Brain Injuries one Frozen Squirrel at a Time

By Silas Aho, WSU Vancouver Neuroscience Student



In the new movie Concussion, which follows the actions of Dr. Bennet Omalu (played by Will Smith), exposes a cover-up by the NFL on players who had suffered traumatic brain injury (TBI). These head injuries are caused by constant collisions with other players, which resulted in players having repeated concussions. Dr. Omalu first became suspicious of NFL players suffering from brain injurys by repeated blows to the head when he performed an autopsy on Pittsburgh Steeler’s Center Mike Webster, who was found dead in his car. What Dr. Omalu discovered was that Webster’s brain was much smaller than usual, an indicator of chronic traumatic encephalography (CTE) which is common among boxers and other players of sports where blows to the head are common. What can happen after repeated trauma to the head are dementia, memory loss, depression and ultimately death. There has been cases recently of players committing suicide and leaving notes or texts asking loved ones to donate their brains to research in order to diagnosis them with CTE. It seems a very sad ending for these players who, looking for a way out of depression, find none and yet try and give an explanation for their actions. Dr. Omalu later sees three other cases of CTE in deceased NFL players, all the while the NFL denies the results of the autopsies performed by Dr. Omalu. The movie obviously dramatizes points of the story but it also brought attention to a problem that not only professional athletes experience but also members of the armed forces and potently any civilian who suffers a strong blow to the head. We don’t really know how many people have CTE, mainly because an autopsy is one of the few ways you can diagnose CTE. However on autopsies of deceased NFL members by the center for the study of traumatic encephalography (CSTE) found that 96% of autopsies performed on NFL members had CTE.

Obviously with 96 out of 100 deceased NFL players showing some signs of CTE the NFL has given somewhat of a resolution on traumatic brain injuries and Dr. Omalu. Currently the NFL has given millions to research and settlements to players and families who have suffered from brain damage on account of the sport. This also has sparked research today on treating and prevention of brain injury. Dr. Kelly Drew of the University of Fairbanks Alaska has been one of these researchers who are looking into treatments of CTE and TBI. Her test subjects, however, are somewhat unconventional. The Artic Ground Squirrel, found commonly in the colder climate of Alaska is a very stout animal that is capable of surviving in very harsh climates, mainly on account of its ability to hibernate. What is interesting from her research is that the artic ground squirrel is immune to traumatic brain injury. This is important because as a hibernating animals undergo extremely cold temperatures they can experience a nearly 90% decrease in blood flow to the brain. That is equivalent to suffering a major heart attack or stroke. What is remarkable is that these hibernating mammals are protected from any brain damage. This has led her and other researchers to investigate why exactly these squirrels don’t seem to be affected by brain damage.

What they discovered was high levels of a chemical called adenosine in the artic ground squirrel that seem to protect their brains from harm. The largest amount of this chemical being seen right before they go into hibernation. This spike in adenosine is not only seen in the artic ground squirrel but also in several other animals that hibernate, such as bears. However, the artic ground squirrel seems to continue this brain protection even after it comes out of hibernation. In a comparison of rats and artic ground squirrels that underwent heart failure that reduced blood to the brain, effectively suffocating it, they found that the rats had greatly increased brain trauma compared to the artic ground squirrel. This means that the artic ground squirrel can protect it self from low blood flow such as stroke, heart failure and strong blows to the head. Dr. Drew has also begun to look into ways of taking the benefits of increased adenosine in the brain and using it for therapeutic treatment. What they found was that rats who essentially were given more adenosine had less brain cell death than rats who did not receive this treatment. Moving forward with these finding From Dr. Drew, and others like her studying the adenosine system, could one day lead to treatments of things like CTE and even stroke. The bulk of which could not have happened with out the help of frozen squirrels.


Lost in Translation

Why do laboratory breakthroughs in pain research rarely work in humans?

By Jonas J. Calsbeek, WSU Vancouver Neuroscience Student

A worried patient walked into a hospital to take part in a new chronic pain clinical trial. A revolutionary marijuana-based medicine shown to be safe and effective in chimpanzee models of chronic pain could be a breakthrough in treatment for everyone from cancer survivors to those suffering with chronic, untreatable pain. The anticipation and excitement in the hospital waiting room was palpable, but short lived. Just 3 days after this treatment, the same hopeful patient was found in a coma, and was declared brain dead shortly after. Six other study participants were also discovered in what was described as a “disturbing” neurological condition following their treatment.

This research was immediately halted by the French government on January 11, 2016, after a company named Biotrial carried out a clinical test using this “revolutionary” drug called Bial. While deaths in these types of controlled studies are isolated, there is a severe lack of translation when it comes to pain therapy research from successful animal models to humans. In fact, the failure rate of pain trials in humans is more than 40% in some studies. So why is it that successful pain-relieving drugs in animal models fail so often when it comes to human trials?

The biggest culprit is how animals are tested in laboratory models of pain. In scientific studies, successful translation indicates that a drug that shows efficacy against chronic pain in an animal model also shows efficacy in human pain patients. In animals, pain is typically measured by recording the time until a withdrawal reflex is observed from a painful stimulus. However, these types of tests are only a measure of evoked hypersensitivity, not an assessment of the functional impact of pain, the aspect of pain patients complain the most about. When people go the doctor with a complaint, they are not placed on a hot plate, nor are they poked at the location of injury to determine the magnitude of the pain. In contrast, the pain is usually reported on a scale from 1 to 10, and the patient describes how much the pain impacts or reduces their ability to engage in typical everyday activities. Humans will often rate themselves in the clinic on this self-report scale, leaving a subjective bias that could influence the reported efficacy of pain therapy treatments.

Ongoing research in Dr. Michael Morgan’s neuroscience laboratory at Washington State University Vancouver involves designing a new method for researchers to assess pain in animals in order to more accurately model how pain impacts people. The lab investigates how chronic pain impacts rodent activity by measuring pain-induced decreases in rotations on a running wheel to see if certain drugs can restore running wheel utilization, similar to the way drugs restore function and activity in human patients. A specialized rodent wheel equipped with a laser beam counts how many times the wheel rotates to give researchers an objective measure of the animal’s preference for normal daily exercise and compare that level to the loss of activity during pain such as migraine, arthritis, or neuropathy. This wheel-running model could change the way novel pain therapeutics are assessed in the animal model before being approved for human trials. Given that pain is assessed in a more clinically relevant manner, Dr. Morgan believes that the translatability of drugs from the laboratory to the clinic should increase dramatically.

Millions of people are desperate for a solution to chronic pain, and researchers are doing their best to respond to the need for advancement in the field of pain management. One promising approach is to accurately model chronic pain by assessing the impact on functional behavior as opposed to pain reflexes, as pain reflex can actually occur in animals without a brain! Advancements in the way pain is assessed in animal models can also improve the accuracy and translation of a variety of experimental compound under investigation for the treatment of chronic pain from preliminary trials to clinical studies. Someday, another hopeful volunteer might walk into another revolutionary chronic pain trial, only this time being confident that they will receive a medication that can improve their quality of life, rather than one that will diminish it.

 Can Overactive Neurons Lead to Development of Alzheimer’s Disease?

By Carolyn Dudko, WSU Vancouver Neuroscience Student

Do you know of anyone who is sick with Alzheimer’s disease? I did. Alzheimer’s patients lose their memories, forget names of loved ones and important events. They forget how to eat, walk, dress, and take care of themselves. Alzheimer’s turns a grown adult into something of an incompetent infant. These symptoms are all caused by damaged neuron connections. Current treatments only treat anxiety, depression, anger and sleeplessness. These treatments only help to increase the quality of life and help caregivers take care of the patient. There are drugs out there that help slow down the symptoms, but no treatments to cure current Alzheimer’s patients and prevent Alzheimer’s symptoms from appearing in other patients.

Studies show that before symptoms appear in Alzheimer’s patients, there is a spike in neuron activity. This spike is seen as a burst in electric activity. This spike in activity is then followed by a production of a toxic protein called Amyloid-β. Amyloid-β is the leading cause of Alzheimer’s. The buildup of the protein creates plaques; these plaques are like a sticky residue that covers the outside of the neurons. The Amyloid-β plaques damage neuron connections around them, which leads to the symptoms associated with Alzheimer’s.

A study was carried out in January 2016 by Yuan and Grutzendler of Yale University in which they set out to find whether manipulation of neuron activity affects production of the Amyloid-β protein. They created two groups of mice, in one group they reduced the amount of neuron activity and in the other group they increased the amount of neuron activity. The researchers manipulated neuron activity by either hyperpolarizing or depolarizing the cells. In hyperpolarization the neurons are made more negative, reducing the activity. In depolarization the neurons are made more positive, increase the activity.

They found that in the group with increased activity there was an excessive amount of Amyloid-β produced and there was extensive neuron damage surrounding the protein plaque. In the group with the reduced neuron activity, Amyloid-β production was prevented and there was no neuron damage.

Researchers want to use this technique in the future to manipulate neuronal activity in potential Alzheimer’s patients. By reducing neuron activity, Amyloid-β production will be prevented and damage to the neurons would be prevented as well. By preventing Amyloid-β production and damage to the neurons, Alzheimer’s symptoms will be prevented. This new technique would finally be a cure for the disease. Instead of stalling and slowing down the symptoms, we can prevent them permanently.

Can Research Exploring a Rare Genetic Disease Help Us Better Understand Alzheimer’s, ADHD, and Chronic Pain?

By Miranda Durst, WSU Vancouver Neuroscience Student



We’ve all been annoyed and distracted by some form of pain, whether minor such as a dull headache or a paper cut or something more major like a broken arm. While experiencing the throbbing pain of smashing my finger in the bedroom door, I imagined how amazing it would be to not feel pain. It is easy to envision the benefits of a life free of discomfort, some people, however, understand all too well what it means to never experience pain of any kind and their lives are very different than what you would assume.

Congenital Insensitivity to Pain with Anhidrosis, or CIPA for short, is a rare genetic disorder where individuals are born unable to feel any type of pain, no matter the circumstance. Sufferers are also not able to sweat, which may sound great especially on a first date or during an important presentation but this makes it very difficult for them to control their internal body temperature. People with CIPA also commonly have learning difficulties; many are mentally retarded, and have trouble controlling their emotions.

New research out of Japan, performed by Yasuhiro Indo, focused not only on the causes of CIPA but how it may be linked to other diseases such as Alzheimer’s and Attention Deficit Hyperactivity Disorder or ADHD. The common link is a chemical known as neuron growth factor. Neuron growth factor is especially important during fetal development because it assists new neurons to grow and form correctly. The neurons that rely on this chemical are found virtually everywhere; in the skin, blood vessels, joints, teeth, organs, and muscles. They are the wiring that connects the brain to the rest of the body. These neurons are especially important for alerting the brain to tissue damage or swelling. However, if the neuron growth factor is not present in the right amounts or at the right times during development these neurons die, cutting off this key communication between the brain and the body. The pain signals communicated by these neurons are also very important for young infants to learn what types of behavior should be avoided to stop them from hurting themselves. For example, infants with CIPA commonly bite off their lips and tongue, or chew chunks off fingers and toes because there are no signals present to alert their brain to the damage they are doing.

Imbalances in neuron growth factor have also been linked to other conditions, such as learning disabilities, emotional issues, Alzheimer’s, and ADHD. Patients with CIPA can help us to better understand the importance of neuron growth factor and the disorders it can cause because they have lost so many key neurons due to this imbalance during fetal development. Additionally, because the routes that their bodies use to send pain signals to the brain are highly damaged, they offer vital insight into normal pain responses in healthy individuals. This creates immense potential for CIPA research to help scientists better understand what causes pain and how to better treat it, giving hope to the public for new innovative treatments for long term chronic pain.

 A Cure for Addiction: Is It Out There?

By Angela Gonzalez, WSU Vancouver Neuroscience Student

Cocaine. Addiction. In 2006 The National Survey on Drug Use and Health reported that cocaine addiction effected 35.5 million people 12 and older. Why is the age 12 included? Do people really start out that young? Can we undo it, and ultimately eliminate addiction? Frantic mothers, fathers, children, and friends ask themselves these question as a loved one suffers from this disease. Is there a cure?

Curing a disease is a complicated recipe. It’s not like baking a pie, where wham bam out comes a sweet smelling dessert. It takes time, sweat, and tears of scientists working day in and day out just to open a small door that is so far away from the ultimate goal. Piece by piece an ingredient is determined, and a large victory is celebrated for the smallest pinch of finding that cure.

A pinch from a large recipe; Perineuronal nets (PNNs). These are like the peel around an orange, it protects the juicy core as it develops and supports so the individual slices can’t fall apart and create an unstable environment for the rest of the orange. Likewise, PNNs surround and protect the cells in our brains, supporting and nurturing them. They are very important for assisting a developing brain, and neuroplasticity, a fancy term for saying our brain can change. Having a plastic brain is important in helping us remember bits and pieces of our lives like learning how to ride a bike, and remembering how to do so later because our brain changes as we learn something new.

According to the NIDA, 1.6% of 8th graders, 2.7% 10th graders, and 4% 12th graders will have used cocaine at least once. Our PNNs will remember trying cocaine for the first time as a youngster, and change some connections in our brains, or make some stronger.

A recent study by Slaker et al. established that cocaine induces plasticity in rats. This means our brain becomes more capable of changing with the use of cocaine. Our brain will change around a new habit- cocaine. Well, what about children whose brains are still developing? Does cocaine use at 12 years old influence plasticity?

A current cohort study at Washington State University looks into development of PNNs in adolescent rats. Because their PNNs are not mature, or even present, it cannot be determined if cocaine will induce plasticity, but it can be seen how they develop through exposure to cocaine.

It is thought that PNN intensity or numbers might be increased in rats receiving cocaine compared to a control group receiving only saline. If this is true, neuronal plasticity will be reduced in rats receiving cocaine in comparison rats receiving saline. These data, if accurate, will open new doors for understanding the development of addiction.

The effect of cocaine has never been observed in developing PNNs. However, we can look at a similar study by Chen et al which relates a different, but analogous kind of addiction: Alcoholism and binge drinking (drinking large amounts over a short period of time) in mice in late adolescence- young adulthood. Repeated binge drinking increased PNNs. Chen notes that increased PNNs resulted in limited neuronal plasticity. These findings “might have implications for the development of compulsive alcohol use”.

Understanding the developmental complications of the brain from repeated cocaine exposure as an adolescent will complete the ingredient for addiction. If the development of addictions is outlined, we may have the recipe. A cure for a deadly disease that effects so many every day, and a perfect pie will come out of the oven.

Mind Control in the 21st Century: Humans, Animals, and Robots

By Jonas Calsbeek, WSU Vancouver Neuroscience Student


imaginingtheinternet. files.wordpress.com

What if you could communicate with your best friend using only thought, without saying a word? What if we could communicate directly with one another through brain waves alone? Vast amounts of time and energy go into studying or learning languages, when a simpler answer might be right at the doorstep. Recent developments in neuroscience research have opened the door to a world of possibilities where brains cooperate with computers to allow direct communication between humans, animals and machines without the need for Rosetta Stone® or brain surgery. These breakthroughs include human brains communicating with another across the internet, directly controlling an animal’s movement and controlling a bionic limb connected to the central nervous system. Imagine the ability to control a prosthetic limb using only thought, and how this technology could change the future of bionics.

Click here to download the full story.



The Science of Love; a Cocktail of Chemicals

By Aleksandra Tsytsyn, WSU Vancouver Neuroscience Student

 Love is one of the most powerful human emotions we face, and probably the one we think about most often. It can unite us to other people in the form of companionships, friendships, and romantic relationships. We see love throughout all of our culture; the millions of romantic comedies that are released around Valentine’s day, the dire need for our daughters/sisters/selves to have a date for prom, the importance we place on marriage, commitment and friendship. Although love is traditionally thought of as having a home in the heart, we can thank our brain for the effects of love that we feel. Having a continual desire for closeness, reduction in anxiety and fear, feeling of euphoric happiness, loss in appetite, and increase in sweating and trembling can all be attributed to the signaling chemicals (neurotransmitters) in our brain. A few key neurotransmitters involved in the chemistry of love are dopamine, oxytocin, and endorphins.

Keep reading about the neuroscience of love!


Stay Healthy, Make Social Connections

By Porsha Beatty, WSU Vancouver Neuroscience Student

The doctor has just walked in. He’s taken a look at your chart and found hypothalamic-pituitary-adrenal activation—the portion of the brain that talks to your body about maintaining balance. In addition, there also seems to be a decrease in your body’s immune system.

“What?” you ask. “I’m active,” you inform him, “I making healthy life choices, I….”

But before you continue, the doctor tells you that is not all; he continues to tell you that because your immune system is lowered, your lymphocyte sensitivity—the cells in of your immune system—has also dropped.

You’re stunned. He tells you this is what often happens during perceived social isolation. You thought you were doing it all right. Occasionally, you do feel a bit down and a lack of drive for life, but really? Does perceived social isolation really cause all of this?

Click to read about social isolation


Ketosis on the Epileptic Brain

By Silas Aho, WSU Vancouver Neuroscience Student

 I’m sure some of you reading this paper may remember a diet in the early 2000’s called the Atkins diet that was based on eating a diet high in fats/proteins and low on carbohydrates. This diet worked by switching the main fuel your body used (carbohydrates) to a new fuel source (fats/proteins). What is amazing is that although this diet was part of large diet craze focused on weight loss it could be also used for treatment of epilepsy, a debilitating neurological disease. The success of this diet as an epilepsy treatment centers on one kind of main molecule: Ketones or specifically ketosis.

Read more about ketosis and epilepsy


Should kids be ‘sleeping their life away’?

By Courtney Miskell, WSU Vancouver Neuroscience Student

After hustling through a daunting checklist of daily duties we peek up and see a sleepy adolescent emerging from their bedroom after sleeping well into the afternoon; ‘You are just getting up? You’re going to sleep your life away!’ Children could be much more productive if they started their daily earlier, right? On the contrary, modern researchers are suggesting that due to the body’s internal time clock that regulates the sleeping cycle, the Circadian rhythm, adolescents are not as cognitively inclined in the earlier hours of the morning leading to a lack of focus, inattentiveness and an increase in anxiety disorders in today’s youth.

Learn about circadian rhythm and a possible link to ADHD!


What makes a person unique?

By Michaela Dunn, WSU Vancouver Neuroscience Student

What accounts for the differences in thoughts, emotions, and behaviors among individuals? This is a critical question in the field of personality neuroscience, and dispute still exists regarding the answer. The way a person generally thinks, feels, and behaves is loosely defined as their personality, and it largely affects an individual’s ability to function in social contexts and in other parts of life.  There are 5 “big” traits that can be used to concisely summarize the way a person thinks, feels, and behaves. These traits are Extraversion (experiencing positive emotion), Neuroticism (experiencing negative emotion), Agreeableness (considering others), Conscientiousness (following rules), and Openness/Intellect (the ability to conceptualize). By considering only these “big” traits as opposed to an entire spectrum of possible traits, scientists are consequently able to more narrowly focus on the predictors of personality.

How do nature and nurture influence personality?


The Biology of Anxiety

By Kathleen Darling, WSU Vancouver Neuroscience Student

In the United States, the most prevalent group of mental health illnesses are anxiety disorders, with 18% of adults self reporting being affected. It comes in many forms that people are likely aware of, like social anxiety or other extreme phobias, as well as some people my not associate with the simple “anxiety” label, like post traumatic stress disorder. With such a saturation of these disorders in the population, it is beneficial to understand how they affect people more readily, as well as how these diseases can be combated in a healthy and productive way for the people afflicted. It is generally accepted that anxiety stems from the innate fear response, present not just in humans, but in all animals. Often categorized as the flight half of the “fight or flight” response, it is the direct result of activation of the sympathetic nervous system.

Keep reading about the sympathetic nervous system and anxiety


Marijauna: Cannabinoid Reception in the Brain

By Levi van Tol, WSU Vancouver Neuroscience Student

Books, movies, songs, politics, schools, and just about every corner we turn to, marijuana is a hot topic in today’s society. From hazy smoke to brownies, the plant is in high demand. Since 2007, marijuana use has been on the rise. It is estimated that 18.9 million people were current marijuana users in 2012, which is just under the equivalent of the entire state of Florida. Of the 9.2% of the United States population over the age of 12 that used illicit drugs within the past month, 7.3% were marijuana users. With the legality of marijuana in great debate all over the country, Colorado, Washington, Alaska and Oregon have all passed laws that make marijuana use recreationally and medically legal. If so many people currently use marijuana then why does it face continued opposition? A wide range of research is being done on marijuana’s effects on the brain, but the basic mechanisms are known.

Learn how marijuana affects the brain


Donuts, Exercise, and the Neuroplasticity-Molecule BDNF

By Teresa Straub, WSU Vancouver Neuroscience Student

Every single morning for the last five years you take a morning run, then enjoy a cup of coffee with a donut before you start your day. You figure something about your routine helps you think better. You attribute the benefit to the crisp air and the sugar rush. But what if there is something deeper happening in your brain to super-charge the cognitive function? Exercise and diet affect levels of a protein in the brain, called Brain-Derived Neurotrophic Factor (BDNF), associated with neuronal development and survival in the brain. BDNF expression mediates many pathways within neurons to improve cognitive function, including learning and memory. BDNF protein expression has been shown to be influenced by diet and exercise.

How does diet and exercise affect your brain?  Click to learn more.


Working Memory: How It Works and Why It Is Important

By Kelsey O’Neill, WSU Vancouver Neuroscience Student

Have you ever wondered how you were able to hold a conversation with someone? Have you ever thought about how you can listen to what someone else is saying and think of how that relates to something you’ve experienced? In addition, have you ever wondered why it is that you can recall what someone is saying during the conversation but have a hard time remembering it afterwards? You probably haven’t thought about it much as most brains perform these tasks seamlessly. This process of remembering information in an active setting is called working memory and is so called in reference to the short-term store of memory in computers.

Learn about working memory!


The Basis and Basics of Common Neurological Diseases/Disorders

By Nathan Allen, WSU Vancouver Neuroscience Student

With the population of the world now exceeding 7 billion people, there exist 7 billion people (even taking into account identical twins) who are genetically, and therefore biologically, unique. And yet despite this extreme variation, who can say that they are neither related to, or know, someone who suffers from a neurological disease or disorder? Indeed, confining the neurological ailments strictly to Alzheimer’s disease, Parkinson’s disease, and Major Depressive Disorder doesn’t greatly diminish that number. Alzheimer’s alone accounts for ~70% of dementia cases and approximately 1 in 9 older Americans suffer from Alzheimers. Approximately 60,000 people in the United States are diagnosed with Parkinson’s every year, and around 6.9% of U.S. adults experience at least one major depressive episode each year. Due to the ubiquity of these problems nearly every person either is or has the potential to be, effected by these diseases at some point in their life and thus knowledge of the symptoms is critical. Additionally, understanding the complexity of these problems allows one to see why these are dilemmas that are not so easily solved, and thus why they are still so prevalent.

Click to learn about the neurobiology of these brain diseases


ALS: The Disease behind the Ice Bucket Challenge

By Arthur Serkov, WSU Vancouver Neuroscience Student

Most of us remember the ALS ice bucket challenge that happened last year when people were dumping buckets of ice water onto themselves “for science”. Although a lot of it was people just getting wet, this national trend did help get the word out about ALS, and ended up raising almost $100 million dollars within the month of August alone. Amyotrophic Lateral Sclerosis (ALS) is a rapidly progressive disease that attacks brain cells called neurons, which are responsible for voluntary muscle control. ALS has an incidence of 3.9 cases per 100,000 people, and in 90% of the cases there is no known cause for this disease. Understanding ALS is important to further develop public sentiment about this neurological disease which kills within 3-4 years of onset.

Read more about ALS


Opioids: A Look at Their Side Effects

By Alexander Tran, WSU Vancouver Neuroscience Student

We all feel pain sometime in our life. Whether it is a small cut, a slight bruise or even a broken bone, pain is a natural phenomenon. There are people; however, that experience pain every day. Pain that will last their entire lives. Chronic pain is the most clinically widespread problem affecting over 1.2 billion people worldwide. Opioids, natural or synthetic drugs used to reduce pain, are the most effective treatment for this pain. Although opioids are the most effective treatment for pain, its use is often hindered by the development of tolerance, dependence, and respiratory depression. There are many other side effects with opioid use but how do they arise? What underlies the cause of tolerance, dependence and these other side effects?

Learn more about opiods here


Perineuronal Nets: Protection for Memories

By Priya Kudva, WSU Vancouver Neuroscience Student



French philosopher Descartes once mused, “I think, therefore I am.” Human consciousness is unique among evolved life forms on Earth. We can think, remember, imagine, visualize, deduce, conclude, and expound. These remarkable abilities that humans possess can only be attributed to the brain and its ability to form connections. The core “brain unit” is the neuron – a specialized cell that transmits information via electrical activity.  But there are more than just neurons in the brain. Around the majority of neurons is a net of fibers and chemicals that protect the neuronal connections and prevent them from disconnecting. However, because humans are always learning new information, the connections in our brains cannot be permanent. And yet, these nets keep the structural plasticity, or ability to form and delete connections to neurons, turned down. These nets of fibers found in both the brain and spinal cord are called perineuronal nets (PNNs).

Learn how perineuronal nets help us remember!



A Brain in Balance

How a neurological balance may help with Parkinson’s disease

By Kyle Campion, WSU Vancouver Neuroscience Student

Like many things in our lives there is a balance. You may want more ice cream, but you realize that you would need more exercise to counterbalance those tempting calories. This decision is what helps prevent us from overeating, and possibly becoming overweight. However, many, such as myself, ignore that and eat the ice cream anyway. There are places where a balance must occur, or major consequences, such as being overweight due to extra ice cream, would happen.

Brain images of the stages of Parkinson’s disease. Reuters.com

Brain images of the stages of Parkinson’s disease. Reuters.com

Your brain is one such place. Parkinson’s disease results from an imbalance in a part of your brain called the basal ganglia. There is a direct and indirect pathway to the basal ganglia. Too much on the indirect pathway causes Parkinson’s disease, and too much on the direct pathway causes excessive movement and Huntington’s disease. Cell death in the basal ganglia is responsible for Parkinson’s disease.

Parkinson’s disease is responsible for an estimated $23 billion dollars per year in the U.S., and takes a toll on both the patient’s and caretaker’s well-being. Some notable cases include Michael J. Fox, Olympic medalist Davis Phinney, and Muhammad Ali.

Currently, there are only temporary treatments for Parkinson’s disease. The first is an L-DOPA (levodopa) regimen, which is a precursor to the neurotransmitter dopamine. L-DOPA is taken to compensate for the death of dopamine cells. The second method is deep brain stimulation which uses small amounts of electricity to stimulate the dying region of the basal ganglia to help strike a balance.

L-DOPA is considered the gold standard for Parkinson’s disease treatment; however its effectiveness decreases after 4-5 years of use, according to the University of Maryland Medical Center.

A previous study showed that a decrease in specific dopamine receptors (D3), cellular points where the drug activates, relieved L-DOPA induced sporadic movements without increasing Parkinson’s disease symptoms.

In a new study, researchers from Rutgers New Jersey Medical School have tinkered with the direct/indirect pathway balance in the basal ganglia. They targeted and increased the number of a specific dopamine receptor (D3) in rats. A drug (ES609) was administered to turn on the dopamine receptor. The drug significantly reduced sporadic movement in the rats, which is a hallmark symptom of prolonged L-DOPA use. This study has shown that the drug can preserve the balance in the basal ganglia when there is a high number of this specific receptor (D3) this drug  can ease the symptoms.

However, further testing is required to determine whether or not this drug regimen would be beneficial to Parkinson’s patients. The study’s researchers indicate that this drug could be a new therapeutic approach to treat sporadic movement in Parkinson’s disease and antipsychotics.


Fighting off Fear in Your Sleep

By Alyona Kutsar, WSU Vancouver Neuroscience student

Imagine your biggest fear: snakes, spiders, or water. Now imagine that that fear can be tamed while you are sleeping.

Scientists in Chicago have done an experiment to try to do just that. The study is called “Stimulus-specific enhancement of fear extinction during slow-wave sleep.”

From www.invigocollection.com

From www.invigocollection.com

The study found that the fear response can be reduced when part of the environment in which the fear stimulus appears is presented while the person is sleeping.

In the study, fifteen participants went through conditioning, where something that doesn’t normally produce a fear response is paired with something that does produce a fear response. This is done to make the person produce a fear response to the thing that doesn’t normally produce fear response.

The participants were shown images of neutral face expressions and given four neutral smells to inhale.  Some of the images and smells were shown and given while the fear stimulus, a small electric shock, was delivered to the participants. Thus, the participants learned to associate certain smells with electric shock and produced fear responses to the shock.

Then, one group of the participants went to sleep while the other group stayed awake.

During the slow-wave part of their sleep, also known as deep sleep, the smell that was administered while the participants were receiving the shock was introduced to the participants. Imaging techniques were used to observe the brains of the participants while sleeping.

After waking up, the participants were again monitored for their fear response to the different smells. This data showed that there were differences in brain activity before and after sleeping. There was a reduction in fear response to the smells after the participants had slept.

To confirm that this fear response reduction occurred only after sleeping, the other group that didn’t sleep was also monitored and found that they did not have the same reduction of fear response to the smell as the group that slept. This suggests that the fear extinction is more effective while sleeping.

The scientists of the study proposed two explanations of why the brain is able to reduce fear response when sleeping. One explanation is that the brain changes the memories and emotions to dissociate the fear stimulus, the shock, from the smells. The other explanation is that the brain creates a new memory where the smell is not associated with the shock.

This study is amazing because it seems to show that the brain is able to rework memories and emotions while sleeping which can be used to treat people with paralyzing fear.

So even when you are not consciously aware of it, your brain is amazingly able to tame your fears while you’re sleeping. In the future, the dream of being able to banish away the fear of spiders, snakes, or water might actually become a reality!


Sleeping More is Thinking More

By Sarah Neveux, WSU Vancouver Neuroscience Student

It might seem a little awkward to ask overweight and sleepy people if you could run tests on them, but that’s what a couple of researchers did in 2013 to study the effects of obesity and sleep deprivation on cognitive function, specifically cognitive impairment.

Obese subjects often have impairments in the area of cognitive control while sleep deprivation decreases attention and impairs processing speed and accuracy. These researchers wanted to see if increasing sleep in an obese individual had any effect on attention or processing.

To qualify for the experiment, people had to get less than 6 ½ hours of sleep per night and have a body mass index or BMI between 30 and 55. The researchers tested to see if the cognitive deficiencies were partially reversible by coaching people on a personalized sleep plan to get at least 7 ½ hours of sleep per night.

By the end of the “sleep intervention” study, the group that had increased their sleep had significant increases in general brain functioning, memory, attention, critical thinking and problem solving skills. They also reported less day-time sleepiness. Simply put, they were better able to engage in daily activities despite the cognitive issues caused by their obesity.

While the conclusions from this study weren’t life changing, they were incredibly promising. There will have to be a number of follow-up studies – specifically studying different pathways of cognitive improvement. What was stunning about this study was that the cognitive impairment was partially reversed without the use of pharmacological substances. That is so unheard of in today’s “pill-popping” society; maybe it’s time to give it a shot!

This article is worth noting purely for the fact that it addresses a number of huge issues in America: obesity and poor sleeping habits. The CDC calls insufficient sleep a health epidemic and the National Highway Traffic Safety Administration estimates drowsy driving to be responsible for over 1,500 fatalities and 100,000 crashes every year in the US. The CDC also says that roughly one-third (35.7%) of Americans are obese, with obesity contributing to innumerable health problems. This study and the information it is trying to bring to light, though in its infancy stage, should be kept in the spotlight. Moving from pharmaceuticals to simple pattern interventions could be the health phenomenon of 2014!


Safer Helmets, Safer Sport, Safer Super Bowl

By Aleksandra Tupikova, WSU Vancouver Neuroscience Student

From www.newenglandflagandbanner.com

From www.newenglandflagandbanner.com

Crack, thud, smack. These are the sounds made on the football field when helmets meet at the same place, at the same time. The greatest enemy football players face on the field is not the opposing team, but head injuries. We’ve all recently seen the nature of the rough sport in the 2014 Super Bowl as players slammed into each other play after play.

What will possibly bring down the enemy? Redeveloped helmets.

Although helmets will not completely prevent head injuries, different helmet designs will reduce the risk of injury, making football a safer sport.

Researchers work with Virginia Tech, Dartmouth College, and other colleges to study over 1 million head impacts all of the college football players got over the course of five years. Specifically they look at the head injury rate between two models of helmets, the Riddell Revolution and Riddell VSR4.

A study published in the Journal of Neurosurgery found there is a 54% reduction in head injury risk with the Riddell Revolution helmet compared with the VSR4, shown by a reduction in the incidence of concussions. Concussions, a kind of head injury, occur when there is some kind of hit to the head and the brain jolts inside of the skull and may even hit the skull. This not only may cause damage to the brain tissue itself, but also chemical imbalance in the brain producing the symptoms of a concussion. These include dizziness, headache and confusion. The reduction in concussion risk is due to the helmets ability to slow down head movements after an impact. Thus slowing down head movements after impact prevents the brain from jolting around inside the skull and ultimately prevents head injuries.

Head injuries received during sports may have possible long-term effects like brain damage. And these injuries are not uncommon at all. Just before the Super Bowl Seattle Seahawks wide receiver Percy Harvin got a concussion on the field. According to the study, “Of all sports, football accounts for the highest incidence of concussion in the US due to the large number of athletes participating and the nature of the sport.”

However, changes in the design of helmets can make football a safer sport not only for our favorite teams, but also for the young kids aspiring to be football players. In this way we can sustain the American legacy.


Love is much more than just a kiss: a neurobiological take on love

By Bailey O’Keath, WSU Vancouver Neuroscience Student

“When you fish for love, bait with your heart, not your brain.” As Mark Twain once noted, when we think about love we often times think all our emotions come from our heart, and we should always feel with our heart. But what the tricky part may be is getting our brains to tell our heart what to feel. Or is there really a connection? The human connection between love, the heart and the brain is an extraordinary one. One we may never fully understand. Researchers have been studying the possible neurobiological links in human love and affection for a very long time now, but studies are still being done in order to see really how the brain is involved in these behaviors. What is it exactly that makes our brains “tick” to those that we love or are attracted to? And what do we do once these brain signals communicate with our body?

From betweenz.blogspot.com

From betweenz.blogspot.com

Brain function, when it comes to love and affection, can be very tricky. The differences in gender, duration of love, and culture can all play big roles in the fMRI results when testing human brains. In this Neuroscience article, researchers specifically studied the brains of individuals by using fMRI scans to try to understand the location and activity of brains when they are focused on love and/or affection. Because of all the different variables in the study, it was hard to pin point where these feelings truly come from and what exactly they tell the rest of our body to do.

When testing human brains for love links, patterns of love overlapped regions of oxytocin receptors. These receptor sites are proteins that link to the hormone oxytocin, which is important in signaling these hormones to carry out brain messages. Scientists later found that roles of serotonin, cortisol, nerve growth factor and even testosterone can have affects on love and affection. This shows that all these hormones in our bodies are found in great numbers when doing these studies on love and affection in the brain.

We always make remarks like, “it’s the hormones” when someone is emotional, but really these hormones may be triggering these feelings of love and affection in our brains and then carries them out throughout the rest of our bodies.

I think this article is particularly interesting, especially since Valentine’s Day is right around the corner, but it can also teach us many new things about love and our brains. Although the connections between our brains and love are not completely clear, it really makes you think about the emotions that we have and how we portray them throughout the day. Love and affection are just some of the emotions that the brain controls, and even though we don’t know exactly where they are coming from in the brain, it is still really important and fascinating that the brain has all this power!

It is important to learn these sorts of things about the brain because we are able to learn more about the brain and ourselves. The more we learn about the human brain, the easier it will be to treat diseases and disorders of the brain. In this case, doctors would be able to help treat hormone level disorders in brains if we knew more about the location and function of where our feelings really come from. We are making progress in brain research, but there are still many more interesting things to learn.

This study done in 2012 may give insight to other studies to be done in the future, and maybe that’s what this Neuroscience article wanted us to think about. Or maybe they just wanted us to feel something. In our brains.


Scared of losing your hand to an elevator door?

By Cameron Elde, WSU Vancouver Neuroscience Student

From clicket.com

From clicket.com

What do Captain Hook, Luke Skywalker, and J.K. Rowling’s Peter Pettigrew all have in common? That’s right, they’re all sporting prosthetics. Captain Hook may have gotten the short end of the stick this time, but modern medicine today can replace limbs better than ever before. Maybe this doesn’t come as a surprise to you; Frankenstein may have been written in the 1800’s but they certainly didn’t replace limbs back then. An article by Brian Carlsen et al., brings to light the recent strides in the fields of prosthetics and rehabilitative surgery and how frequently they work in tandem.

From Carlsen et al. 2013

From Carlsen et al. 2013

When considering how far prosthetics have come it seems to cross into science fiction. Myoelectric prosthesis function by detecting movement in the muscles that exist in the remaining limb. Moving these muscles makes the prosthetic move as well. That being said it is very important for the prosthetic to be able to feel the muscles underneath, creating the need for some surgeries explicitly to get more functionality out of these prostheses. Operations to lengthen remaining limbs to better attach prosthetics to, or to bring the muscles closer to the surface of the skin are both commonplace.

Many fields of medicine, including prosthetics and rehabilitative surgery have made tremendous strides in recent years. However, while each field holds promise on its own, the best approach to limb loss takes multiple directions. Take the case of one 36-year-old man who lost much of his right hand in an industrial saw accident. With only his thumb and one exhausted functioning finger remaining, some form of intervention was needed. The best option was neither entirely surgical, nor prosthetic. The non-functioning finger was amputated and parts of the palm along with the missing fingers were replaced with myoelectric prosthetics. This opportunity however, was only realized through the collaboration of a trio of specialists including a prosthetist, therapist, and surgeon. This procedure resulted in a functional hand, but most importantly, a satisfied patient.

Even when considering the amazing potential when surgery and prosthetics team up there is another even more exciting possibility on the horizon: hand transplantation. Previous attempts have struggled due to immune systems rejecting the transplant. New immunosuppressive techniques however, help to mitigate this hurdle. While existing as a potential treatment, this procedure remains highly controversial and debates upon its ethicality are heated. Why support such a procedure with considerable health risks when conventional prosthetic options exist? One of the key factors in determining what amount of functionality will return following transplantation is nerve regeneration. The difficulty with predicting the level of regeneration however, prevents this technique from having consistent results.

As the field of medicine grows we find ourselves capable of things never before possible. It’s important though, not to lose perspective of the true goal: restoring the person.


The Brain Beat You to the Punchline: How Neural Activity Helps Mediate Humor

By Nicole Smith, WSU Vancouver Neuroscience Student

Terry Gilliam’s hallmark Monty Python animations- cartoons that audiences may find more or less funny based on their expectations rather than the comedic merit, according to a new study

Terry Gilliam’s hallmark Monty Python animations- cartoons that audiences may find more or less funny based on their expectations rather than the comedic merit, according to a new study

“Observe due measure, for right timing is in all things the most important factor.” –Hesiod, Greek poet, ~700 BC

Hesiod’s sentiment of caution is echoed as the ubiquitous unwritten rule of comedy: Timing is everything. A recent study published in PLoS One suggests that, within the brain, this comedic timing may be imperative. The article, entitled “Decoding Humor Experiences from Brain Activity of People Viewing Comedy Movies,” details an investigation into the patterns of human brain activity in an fMRI machine, in response to stand-up comedy performances. fMRIs are commonly used to detect changes in the brain’s blood flow surrounding certain behaviors or activities, and thought to be indicative of activity. The Tokyo based research team then developed computerized decoders they call “humor detectors.” Like something out of a sci-fi movie, humor detectors detect not only the presence of humor processing by the brain, but the timing at which this processing occurs (i.e., before, during, or after the onset of a joke).

The experiment tested 9 participants by placing them each into an fMRI machine and subjecting them to taped stand-up comedy routines, during which their brains were scanned and they used a device to indicate their sensation of humor. A 10th participant’s brain was then scanned, and compared to the other 9 scans. Using this data, the humor detectors accurately determined the onset of the 10th participant’s humor perception. As the authors note, “Such physiological measurements for experiencing humor should be of value to the creators of comedy shows and movies, because it would help them to know the detailed reactions of audiences and the objective value of their products.” Taking a cue from Hesiod, they also highlight the importance of giving viewers a punch line within seconds of their expectation to maximize laughter, stating, “Our results provide evidence that there exists a mental state lasting for a few seconds before actual humor perception, as if a viewer is expecting the future humorous events.”

So, is it the punch line that has comedic value, or the time at which it hits you? Furthering the team’s support of the latter, they found that brain areas such as the prefrontal and temporal cortex were particularly active before the perception of humor. These regions have been connected with the ability to infer mental states of others, as well as understand speech within specific contexts, suggesting that a viewer laughs when an anticipated punch line satisfies their inferred timing.  Understanding the dynamics of humor has universal value to humans, as nearly all cultures have some form of comic relief that, among other positives, helps build social relationships. This study’s spinoffs might address different types of humor in the future, comparing the different brain activity produced from watching, say, Monty Python or The Full Monty, or even comparing reading versus watching comedy. Further, a similar algorithm may be developed as a “drama detector” to analyze the different reactions dramas can elicit.


Withholding Sleep Tips the Brain’s Seesaw

By Teresa Straub, WSU Vancouver Neuroscience Student

Chronic sleep deprivation affects most of us at some point or another in our lives.  Whatever your situation, whether you have constant pressure from the boss to write up more project proposals, a second job to keep with the rising cost of living, night classes, play computer games till 3 am, or lay awake worrying about the problems you face, sleep eludes even the most tired person.  To that extent, sleep is an important topic that may have more implications for our neurological health than we as a society, and researchers, realize.  Sleep plays an important role in maintaining the chemical balance our brains use to function optimally.  Imagine chemicals balance a seesaw in the brain.  When all the chemicals are in the proper concentrations the seesaw is perfectly balanced.  However, if the seesaw is tipped by altering the concentration of the brain’s chemicals, it could affect how the brain works and reduce protection of the brain against harmful activity.  Therefore it is important to understand how sleep restriction affects the cells in our nervous system and our behavior.

Courtesy of weightymatters.ca

Courtesy of weightymatters.ca

“How does staying up night after night to keep up with the demanding workload affect my brain cells?” This is the question addressed by researchers at Tufts School of Medicine in Boston, MA in a recent paper in the Journal of Neuroscience entitled “Chronic Sleep Restriction Disrupts Sleep Homeostasis and Behavioral Sensitivity to Alcohol by Reducing the Extracellular Accumulation of Adenosine”.

This study restricted the sleep that mice received for three days while monitoring slow-wave activity (SWA).  What does this mean? While we sleep, our brains have different activity levels measured in waves.  The deepest sleep is characterized by slow-wave activity (SWA). Monitoring the slow waves in mice brains essentially monitors the depth of sleep the mice undergo.

Also, in our brains we have adenosine, which is a chemical involved in sending communication signals. The concentration of adenosine in our brain affects our stroke risk, epileptic activity, tiredness and quality of sleep, energy metabolism, and regulating body temperature, and has numerous other roles.  The concentration of adenosine in the mice brains was monitored.

After the first day that the mice were deprived of sleep, the body’s homeostatic mechanisms compensated for the lack of sleep by increasing the concentration of adenosine and SWA.  However, this compensation didn’t last long—when the sleep-deprived mice were further deprived of six hours of sleep, their SWA and adenosine levels were reduced for at least two weeks.  This shows the potential long-term impact sleep deprivation may have on the nervous system. Reducing SWA may mean having a lighter, less satisfying sleep, and reducing the adenosine concentrations may affect how well you sleep and if you recover should you have strokes or seizures, among other more regulatory functions.  The sleep-deprived mice also were less sensitive to alcohol after being restricted from sleep for twenty-four hours. This may suggest that the adenosine concentration affects response to alcohol because of chronic sleep deprivation.

This current research, released January 29, 2014, may be important for stimulating future research to identify consequences of sleep deprivation.  One way that this study could affect society is if it is a springboard for further studies, which may find sleep deprivation to have impacts on the nervous system that cannot be masked for long by guzzling Red Bulls and brewing pots of coffee throughout the day.  Identifying the underlying cellular mechanisms affected by chronic lack of sleep may help us understand how to improve cognition and behavior by keeping the brain’s chemical concentration seesaw in balance.  This may have a wide-spread impact on the population trading sleep for progress, and possibly their neurological health.


Balance: On a high-wire and in Neuroscience

By Nicholas Rolig, WSU Vancouver Neuroscience Student

From cdn.slashgear.com

From cdn.slashgear.com

You are in Arizona, walking on a two inch thick high-wire (cable) that connects both sides of a canyon, 1,500+ feet in the air. As you walk, step by step, your feet wrap around the flexing cable that sways in the wind. A few minutes into the walk, you feel your muscles starting to fatigue, with some being used more than others. Your life depends on your ability to balance; your ability to activate and inhibit the correct muscles at the right time. At one moment you flex your quadriceps and relax your hamstrings, and the next you flex hamstrings and relax your quadriceps. Not only are you 1,500 feet above the canyon floor, but you are doing this on live TV, with the whole world watching and asking: will he make it?

This is a simplified snapshot of the experience Nik Wallenda, a high-wire artist, when he dared to walk across a canyon near the Grand Canyon. What’s interesting is that Wallenda’s performance near the Grand Canyon is a perfect example to use to describe a few fundamental concepts in neuroscience.

In neuroscience, it has been established that there are two main types of actions one neuron (a brain cell) can do to anther when communicating: excite its neighboring cell by activating it or inhibit its neighboring cell by deactivating it. Depending on the function or process, either excitatory or inhibitory, or a combination of both are used.

From www.baynews9.com

From www.baynews9.com

In the case of Wallenda’s high-wire performance, both excitatory and inhibitory neurons were used when he alternated between using certain muscle groups such as his quadriceps and hamstrings. One example of this could have been when he activated his quadriceps to push his leg down/backwards and relaxed his hamstrings to enable his leg to move. The main idea behind this is that in order to successfully move a leg, one must have both excitatory and inhibitory neurons activated, with excitatory neurons activating the movement associated muscle group, and inhibitory neurons deactivating the muscles preventing the movement. It is with the balance of both excitatory and inhibitory neurons that we are able to move our legs, such as what Wallenda did when we walked the cable.

In a recent study, Sally A Marika and her colleagues provided evidence that this balance between excitatory and inhibitory neurons not only occurs between the interactions of neurons and muscles, but showed the presence of both neuron types within the eyes of monkeys.

In Marika’s study, she and her colleagues found that when the monkey’s eyes were damaged via a cut in the retina (the most inward part of the eye where light gets absorbed though the pupil and converted into signals for other neurons), both excitatory and inhibitory neurons took part in the repair process. They determined this over a course of two studies, by specifically observing the growth of both excitatory and inhibitory neurons via a microscope and neuron specific (either excitatory or inhibitory) florescence dye; the most recent study observing inhibitory neuron growth.

Similar to how Wallenda’s muscles were activated or inhibited by the activation of excitatory and inhibitory neurons, Marika and her colleagues hypothesized that both excitatory and inhibitory neurons are both necessary to see.

In the end, Nik Wallenda seems to not be the only one balancing. Rather, it appears that balance is a reoccurring idea in neuroscience. From the activation and inhibition of muscles, to the functions of a monkey’s eye, balance seems to be a key idea.