Stress Relief Through Physical Exercise

           We hear everywhere, on social media, in the news, and at annual medical appointments, that physical exercise is essential for our health. We are told that it can improve our mood, reduce stress, build muscle, manage injuries, and help us remain independent as we age. However, these are just familiar statements that leave the questions unanswered… How does exercise make us feel better, and most importantly, when should we expect those benefits, tomorrow or in a few years? Instead, the reality is quite different, some people feel sore and exhausted after a workout rather than energized and happy, and there aren't many conversations about this side of physical activity.

Countless studies and articles address this topic. And these questions made me want to find evidence that physical activity could really bring those benefits. During this semester's neuroscience seminar, Dr. Buhr gave a talk about his research called “The persistence of stress-induced physical inactivity in rats.” He found that rats exposed to stress showed a lasting decrease in physical activity (specifically wheel running). And after reading that study, I wondered how different it might be in humans, since physical activity is supposed to help us cope with stress. During my research, I came across an article called “Exercise fends off middle-age stress, study shows” published in January 2026. The study followed 3,300 adults aged 31 to 46 years old in Finland. The researchers found that participants who remained physically active had lower stress levels than those who remained insufficiently active. I also find this age range best for research on physical activity since many people by age 30 already have established work and home schedules that shape their activity level and habits. It's also important to mention that the human study and Dr. Buhr's experiment examine quite different relationships between stress and physical activity. The human study focuses on activity level associated with stress burden, while Dr. Buhr's experiment shows that (intentionally caused) physical stress reduces the desire for physical activity in rats. Additionally, some studies involving people diagnosed with PTSD also show decreased physical activity. Together, these findings suggest that it can be challenging for people already living in a high stress environment to increase their physical activity, which might actually help them manage stress. However, the study in Finland supports the idea that physical activity can help people cope with stress.

In my personal experience, I had to find an activity I enjoy enough to maintain a sufficient activity level. I'm prone to procrastination, but I have noticed that after exercising, I often feel more energetic and ready to complete other tasks. However, that usually happens only after I do a physical activity I enjoy, like walking, and if I have to do something I don't really like, such as certain household chores, the effect on my energy level feels the opposite. This experience has shown me how important it is to find something that I enjoy. That way, I can appreciate the process itself while working towards my goals.

 

Citations:

1.       Exercise Fends off Middle-Age Stress, Study Shows, www.usnews.com/news/health-news/articles/2026-01-27/exercise-fends-off-middle-age-stress-study-shows. Accessed 13 Oct. 2026 .

2.       Buhr TJ, Reed CH, Wee OM, Lee JH, Yuan LL, Fleshner M, Valentine RJ and Clark PJ (2023) The persistence of stress-induced physical inactivity in rats: an investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress. Front. Behav. Neurosci. 17:1169151.

The effects of stress on exercise and physical activity

 

Now You See It, Now you Don't: How Perception Plays Into Reality

 In elementary school, there was probably not much thought when it came to understanding how our brains worked. From playing connect the dots or Pictionary, our perception was dictated by our limited experiences on Earth. Looking back on our early childhood days, have you wondered how at such a young age we were able to recognize complex shapes, with such limited lifetime experiences? Without having to pick up a lesson book to teach us how to perceive, we just did it, but now it is time to understand how it actually works. 

As it reveals, everyday experiences and stored memories dating back to our childhood days can reveal fascinating revelations about the human brain and how our perception isn’t always based on what we see, but how we interpret what we see. 

In Dr. Nick Baker and Dr. Philip Kellman’s research article, Shape from dots: a window into abstraction processes in visual perception, they explore the concept of separate dots and how they can be perceived as coherent objects in the visual system. They do so by conducting a series of four separate experiments, all achieving different goals to test the visual system. In experiment 1, they test the contour perception of shapes, concluding that dots within surrounding areas of each other can influence whether or not an object is seen as smooth or curvy. In experiment 2, the rate of the shapes is tested, relating back to experiment 1, where the smoother/ more curvier shapes are perceived more coherently than the shapes with a sharper outline. Experiment 3 and 4 they conclude that within these complex arrays, the smoother shapes are easily perceived and compared across different shape orientations.

You might be wondering where this connection can bring us into the world of Neuroscience, but visual perception leads to many doors that are waiting to be opened. More specifically, as young college students, the use of drugs is prevalent within this generation, especially the use of psychedelics. Psychedelics are a 5-HT2A receptor antagonist that binds to the receptor and influence the visual perception of the individual. This is observed in Dr. Whites research in the article; How Psychedelics alter perceptions: A glimpse into the brain’s inner world. In this research it is investigated how these psychedelic substances are able to influence the neuronal activity across different brain regions that are associated with visual processing and memory. The way they tested this was through studying awake mice and observing their neuronal activity through optical imaging. The visual cortex and retro splenial cortex were observed closely revealing that after administration of the psychedelic, the number of 5-Hz oscillations increased to repeating to five times per second. This means that the receptors were increased in spontaneous firing and shows the influence in visual processing through this substance.

Whether it is through the visual processing of shapes through filling in the gaps of dot arrays or understanding how perception changes through the use of drugs. Perception is ever changing and a non-linear idea with no one correct answer, demonstrating the complexity of the brain. 

 

 

                                                               Works Cited

“How Psychedelics Alter Perception: A Glimpse into the Brain’s Inner World.” News, 13 Feb. 2026, www.news-medical.net/news/20260213/How-psychedelics-alter-perception-A-glimpse-into-the-brains-inner-world.aspx.

Baker N and Kellman PJ (2024) Shape from dots: a window into abstraction processes in visual perception.
Front. Comput. Sci. 6:1367534. 

doi: 10.3389/fcomp.2024.1367534 

 

The Neurotransmitter Behind Your Abandoned Gym Membership

     We’ve all heard the traditional New Years Resolution of “consistently working out” and the subsequent mass cancellation of gym memberships mere months later. However, the lack of motivation to be physically active might not just be an issue of sheer will, but rather one that is impacted by one’s lifestyle and their environment.

    Buhr et al. (2023) focused on how stress lowers motivation to participate in voluntary activity. His hypothesis was tested by giving groups of rats access to a running wheel and then exposing them to 0, 50, or 100 tail shocks. The shocks served as a stressor, and the wheel stayed locked until 36 hours after shock administration, when the rats were given free access and observed. The rats that were exposed to more shocks had persistent deficits in wheel running that lasted more than 40 days. This behavioral effect was limited to voluntary behavior specifically because all the animals recovered normally on forced exercise tasks such as a forced swim test within 72 hours. To examine how brain chemistry might explain this behavior, rats were sacrificed in order to compare differences in neurochemicals between each group. Within the prefrontal cortex, non-stressed rats had a higher rate of dopamine turnover, (how quickly dopamine is used and then replaced), which could mean that voluntary activity is more rewarding. Within the striatum, a region deep within the brain involved in movement, reward and decision making, the animals that were exposed to more shocks had lower levels of dopamine but similar levels of dopamine usage, which implies that stressed animals have a smaller reserve of dopamine to draw from. This biological deficit provides a potential explanation for why it is harder for stressed rats to stay motivated when performing voluntary tasks.

Friend et al. (2017, Cell Metabolism) examines a similar principle of how dopamine impacts movement and activity levels but this time through the lens of obesity. In the study mice were fed either a normal or high-fat diet for 18 weeks. High-fat mice started gaining weight after 2 weeks and then became less active after 4 weeks. Looking within the brains of these mice, the primary neurological difference was in the D2 dopamine receptors. Within obese mice there was less binding of D2 receptors despite similarities in the amount of dopamine and the dopamine-producing enzyme, tyrosine hydroxylase. Gene activity within the D2 receptor gene and the total amount of D2 protein was also similar among both groups of mice. Given the similarities in other receptors and the aforementioned levels of dopamine and enzymes, it was hypothesized that D2 receptors were less available or less functional rather than being in shorter supply within obese mice. Because the  only difference was in the binding of dopamine to the receptors rather than the genetic activity or level of dopamine itself, the function of D2 is the most reasonable explanation for the differences in behavior. The overall firing rate of neurons within the striatum was normal within obese mice; however, fewer neurons turned on during movement with 19% of striatal neurons turning on in obese mice during movement in comparison to 58% in lean mice. Within indirect pathway medium spiny neurons (iMSNs), neurons that can act as a brake on movement, changes were made to further examine the effect of the D2 receptor. When D2 receptors were removed from iMSNs, lean mice became less active. When iMSNs were inhibited using DREADDs, obese mice became more active.

Both of these studies examine how dopamine affects the motivation to perform physical tasks but through different lenses, one focusing on dopamine and the other focusing on the broader pathway and the function of dopamine receptors themselves rather than just the neurotransmitter.

 The fact that there are a variety of ways for dopamine to impact the desire to move shows how crucial a part it plays in our ability to interact with the world around us. Additionally, the biological backing for inactivity shows just how intensely one’s environment can impact their lives down to the most basic neuronal level. I would be interested to examine the role of dopamine through the linkage between stress and weight gain and see how the research done in both of these papers interacts to affect motivation and movement.

Citations

Buhr, T. J., Reed, C. H., Wee, O. M., Lee, J. H., Yuan, L.-L., Fleshner, M., Valentine, R. J., & Clark, P. J. (2023). The persistence of stress-induced physical inactivity in rats: An investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress. Frontiers in Behavioral Neuroscience, 17, Article 1169151. https://doi.org/10.3389/fnbeh.2023.1169151

Friend, D. M., Devarakonda, K., O’Neal, T. J., Skirzewski, M., Papazoglou, I., Kaplan, A. R., Liow, J.-S., Guo, J., Rane, S. G., Rubinstein, M., Alvarez, V. A., Hall, K. D., & Kravitz, A. V. (2017). Basal ganglia dysfunction contributes to physical inactivity in obesity. Cell Metabolism, 25(2), 312–321. https://doi.org/10.1016/j.cmet.2016.12.001

How Understanding Brain Receptors Can Help Us Treat Alcohol Addiction

Before Dr. Hoffman's presentation, I had the impression of alcohol addiction as an issue regarding cravings, behavior, and complications in controlling alcohol consumption. Although I did have an understanding that addiction has a significant effect on the brain, I did not take into account how specific receptors involved in communication between neurons could also be a factor in drinking behavior. Dr. Hoffman's research made me perceive that alcohol use disorder isn't only about an individual's choice. More specifically, it involves biological differences that could help explain why continuously drinking alcohol can be an incredibly difficult task to quit. 

One aspect of Dr. Hoffman's research that caught my attention was her investigation of AMPA receptors. These receptors respond to glutamate, an excitatory neurotransmitter that helps neurons communicate with each other. AMPA receptors play a role within memory, learning, and changes in the strength of connections between neurons. This happened due to alcohol affecting these signaling pathways; researchers are intrigued to unveil whether targeting particular AMPA receptors could gear towards the solution of reducing excessive drinking, 

Within Dr. Hoffman's research paper, she and her colleagues investigated a compound called JNJ-55511118, which inhibits AMPA receptors associated with a regulatory protein called TARP y-8. They examined whether this compound could diminish alcohol self-administration in mice. The researcher discovered that the treatment drastically reduced alcohol-reinforced responding within male mice; however, they did not reduce the response for a sucrose-only reward. In comparison, the same treatment did not produce the same outcome in female mice. This difference truly amazed me, since it suggests that a treatment targeting precise brain mechanisms may potentially not work as effectively in every biological group.

Siddiqi et al. (2023) penned a research article titled “Prefrontal cortex glutamatergic adaptation in a mouse model of alcohol use disorder” that grabbed my attention regarding this topic. Some researchers at institutions such as The Scripps Research Institute and Binghamton University conducted this study. The researchers analyzed how excessive alcohol exposure and withdrawal substantially affected AMPA receptor function in the medial prefrontal cortex of male mice. 

The prefrontal cortex is known as the executive control center, which is involved in behavioral control, decision-making, impulse control, and focus. Using a mouse model of alcohol dependence, the researchers observed increased AMPA receptor-mediated excitatory signaling in the prefrontal cortex. Furthermore, they also recognized reduced expression of specific genes that were associated with AMPA receptor subunits and synaptic plasticity during withdrawal. This indicates that alcohol dependence can alter neuronal communication in complex ways, even when few molecular measurements point in the opposite direction. 

What caught my attention was the distinction between the two studies. Dr. Hoffman's research studies whether selectively inhibiting specific AMPA receptors could lower alcohol-seeking behavior. Whereas Siddiqi and colleagues assessed how being dependent on alcohol alters AMPA receptor function. The outside article was remarkably intriguing because AMPA receptor-mediated signaling decreased even though certain receptor-related genes decreased. When I first read these findings, I felt slightly confused. However, these outcomes suggest that changes in gene expression do not necessarily reflect how intensely receptors function. Both of the studies show why comprehending addiction needs examining both routes: functional and molecular changes that occur within the brain.

These conclusions could help researchers to develop refined treatments for alcohol use disorder. Knowing and understanding how alcohol changes AMPA receptor activity can result in treatments that account for variation in sex and drinking history. However, this may make it difficult to determine whether these findings apply to humans. Since Dr. Hoffman's study discovered various responses in female and male mice, further research may reveal whether sex also has an effect in how the brain responds to alcohol and addiction treatments. 

Overall, Dr. Hoffman's presentation gave me insight about alcohol addiction from a biological standpoint. In addition, the outside article reinforced that insight by demonstrating how chronic alcohol exposure can modify AMPA receptor signaling in a brain region participating in behavioral control. These results raise a question for me about whether a better understanding of how alcohol changes AMPA receptors results in treatments that are more beneficial for different categories of people. 

References 

1. Hoffman, J. L., Faccidomo, S., Saunders, B. L., Taylor, S. M., Kim, M., & Hodge, C. W. (2021). Inhibition of AMPA receptors (AMPARs) containing transmembrane AMPAR regulatory protein γ‐8 with JNJ‐55511118 shows preclinical efficacy in reducing chronic repetitive alcohol self‐administration. Alcoholism: Clinical and Experimental Research, 45(7), 1424–1435. https://doi.org/10.1111/acer.14639 

2. Siddiqi, M. T., Podder, D., Pahng, A. R., Athanason, A. C., Nadav, T., Cates-Gatto, C., Kreifeldt, M., Contet, C., Roberts, A. J., Edwards, S., Roberto, M., & Varodayan, F. P. (2023). Prefrontal cortex glutamatergic adaptations in a mouse model of alcohol use disorder. Addiction Neuroscience, 9, 100137. https://doi.org/10.1016/j.addicn.2023.100137 

GLP-1s: A Possible New Cure for Alcohol Addiction?

     Alcohol addiction, or alcohol use disorder (AUD), is a condition that affects around 29.5 million people in the United States alone, with that number likely being higher due to underreporting and the stigma surrounding addiction. Traditional methods for sobriety, such as rehab, FDA-approved medications, behavioral therapies, counseling, and support groups, may be insufficient, as various individuals relapse or require multiple rounds of detox or withdrawal to break their addiction. Although many traditional methods to sobriety focus on the cognitive aspect of addiction, it is important to recognize the role of addiction on the brain itself.

    In her research, Dr. Jessica Hoffman recognizes the critical role of TARP γ-8 AMPA receptors in AUD and how TARP γ-8 regulates passive, active, and dependence-escalated alcohol self-administration. In her research, Dr. Hoffman and her team discovered a drug called JNJ-55511118, a TARP γ-8-bound AMPAR negative modulator that decreases alcohol reinforcement in certain mouse populations. However, this drug was not successful in all mouse populations, as the drug appeared to have a diminished effect in female mice and did not decrease their alcohol consumption. This further proves the point that not all treatments for AUD are successful and may fail in certain populations, which requires further investigation into which drugs are most effective and whether drug cocktails can be tailored to individuals to help them achieve sobriety.

    These findings relate to an article published in the Journal of the Endocrine Society, GLP-1 Therapeutics and Their Emerging Role in Alcohol and Substance Use Disorders: An Endocrinology Primer. This study had a promising discovery, finding that Glucagon-Like Peptide-1 Receptor agonists (GLP-1RAs) may reduce cravings for alcohol, utilizing the hunger-reducing mechanisms of the medication to act on a similar pathway that fuels addiction. In a more recent randomized controlled trial, it was shown that a low-dose semaglutide (a newer GLP-1RA) reduced laboratory alcohol self-administration in rodent models and in humans. Although this study has some promising results, more research needs to be done on the seemingly connected pathways implicated in addiction and obesity. 

    Both studies show promising results in finding medications that will help those suffering from AUD, and researchers must understand that targeting the pathways or neurophysiology may advance the research to find a more definitive cure or path to sobriety. As we discover new medications that may reduce addiction, it is important to explore and recognize that medications will not work uniformly across all populations, and that the cure to addiction is not a one-size-fits-all approach, but rather an approach that combines medications, therapy, counseling, rehab, and support groups that is tailored to the individual's needs. 

1. Hoffman, J. L.; Faccidomo, S.; Saunders, B. L.; Taylor, S. M.; Kim, M.; Hodge, C. W. Inhibition of AMPA Receptors (AMPARs) Containing Transmembrane AMPAR Regulatory Protein Γ‐8 with JNJ‐55511118 Shows Preclinical Efficacy in Reducing Chronic Repetitive Alcohol Self‐administration. Alcoholism Clin & Exp Res2021, 45(7), 1424–1435. https://doi.org/10.1111/acer.14639
2. Nirupam M Srinivasan, Mehdi Farokhnia, Lisa A Farinelli, Anna Ferrulli, Lorenzo Leggio. GLP-1 Therapeutics and Their Emerging Role in Alcohol and Substance Use Disorders: An Endocrinology Primer. Journal of the Endocrine Society, 2025; 9 (11). DOI: 10.1210/jendso/bvaf141
3. The Endocrine Society. "Weight-loss drugs like Ozempic may also curb drug and alcohol addiction." ScienceDaily. ScienceDaily, 26 October 2025. <www.sciencedaily.com/releases/2025/10/251026021746.htm>.

You're Not Lazy, You're Just Stressed: The Connection Between Stress and Exercise

    Everyone thinks that the only reason why people don't want to workout is because they are lazy, but what's the real reason? What is causing people to stray away and lack any form of motivation to exercise? Well, it is evident that humans are complex beings, so there isn't a single answer to this question. However, one possible answer that is mentioned and is backed by studies is the idea of being too stressed out. According to a study by Buhr et al. (2023) that was done on rats, being exposed to some type of stress or trauma caused a change in the rats' brain chemicals, which in return, made the rats less physically active. Another study by Yoon et al. (2023) that was done on the same topic but with humans found that there is indeed a connection between being stressed out, and a lack of exercise. If we take this all into account, it is safe to claim that one of the most important reasons for someone to become less physically active is being exposed to or is currently going through a stressful event or events.

    The study that was done by Buhr et al. (2023) had two goals in mind. One was to see whether stress actually causes a lack of exercise and if the severity of the stress mattered, and the second goal was to see if stress causes a change in the brain chemistry and a change in how the muscles react during exercise. This was tested by having the rats be electrically shocked, which was their way of creating stress, on their tails using three different amounts: 0 tail shocks, 50 tail shocks, and 100 tail shocks. The results showed that the more the rats were shocked, the less they wanted to exercise. It also showed that their dopaminergic levels decreased, which is responsible for up regulating motivation (Buhr et al., 2023). Lastly, the rats' muscles saw an increase of oxidative stress, which made their muscles fatigue faster (Buhr et al., 2023). In other words, when the rats experienced a traumatic experience, they lost motivation and their muscles could not properly recover quick enough, which made it harder for them to continue exercising.

     Very interesting study, but now I wanted to see if something similar was conducted with humans. The study by Yoon et al. (2023) did exactly that. It is a self-reported study where the researchers gathered three groups of people. One group was for those who reported that their life was filled with "very severe" or "severe" amounts of stress, the next was for those who reported their stress as "moderate", and the last group of people was for those who reported their stress as "slight" or "very slight". There they had each of these groups commit to exercising for 30 minutes at least once a week. The results showed that those who reported "moderate", "very severe", or "severe" amounts of stress exercised less than those who only had "slight" or "very slight" amounts of stress. Essentially, the more stress someone has, the less likely they will want to workout. The study explained that stress reduces motivation, and increases feelings of weakness and fatigue (Yoon et al., 2023). Also, those who are under stress tend to not have an adequate amount of self-regulatory resources, which further makes someone want to avoid any type of physical activity (Yoon et al., 2023).

    Both of these studies are extremely important as they spread awareness to those who believe that their stress won't have a direct negative effect on their activity levels. The problem with not knowing this information will unfortunately allow those people to sink deeper and deeper into their sedentary lifestyle. A sedentary lifestyle is an extremely unhealthy way to live. It causes you to have an increased rate of dying early, lower your energy levels, increase your weight, and your fitness levels will drop as well. This is why studies like these are great as they provide helpful information that will benefit millions of people. 

    Overall, stress is a problem when it comes to wanting to be physically fit. The study from Buhr et al. (2023) found that stress makes someone less motivated and causes their muscles to have a hard time recovering, which will make them fatigue faster than normal. Moreover, the study from Yoon et al. (2023), also found that stress causes a lack of motivation and a sense of feeling weaker and more tired. When you allow the stress to win you over, you won't even realize it, and by then it'll be too hard to get back up. This is why it is important to be educated on the negative effects of being stressed out when it comes to your physical fitness.     

                                                                    References

• Buhr TJ, Reed CH, Wee OM, Lee JH, Yuan L-L, Fleshner M, Valentine RJ and Clark PJ (2023) The persistence of stress-induced physical inactivity in rats: an investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress. Front. Behav. Neurosci. 17:1169151. doi: 10.3389/fnbeh.2023.1169151
• Yoon, E. S., So, W.-Y., & Jang, S. (2023). Association between Perceived Psychological Stress and Exercise Behaviors: A Cross-Sectional Study Using the Survey of National Physical Fitness. Life, 13(10), 2059. https://doi.org/10.3390/life13102059

    

The Normalization of Regular Alcohol Consumption: How much is too much?

  Alcohol consumption in the United States has become something as normalized as grabbing a sweet treat after dinner. A glass or two of wine with a meal every night, a monthly golf trip with stops at the beverage cart at each hole, a weekly outing at a local Mexican restaurant for a five dollar pitcher of margaritas, etc. It seems Americans have somehow managed to find a way to intertwine alcohol into activities that are presumably quite enjoyable without the need for substances at every corner. At some point, it may be necessary to question when regular alcohol consumption becomes an issue–and that point may just be now. 

Dr. Jessica Hoffman of Loyola University Chicago’s Stritch School of Medicine spoke about the dangers of regular alcohol consumption and its impacts on brain function at her talk titled “Alcohol, Plasticity, and Brain Vulnerability”. She informed the audience that nearly ten percent of Americans are diagnosed with alcohol use disorders–and those are just the people who were conscious enough to recognize that they had a problem. With the increase in the frequency of drinking culture in the United States, it is no question that there are likely millions of people who drink more than they should be drinking, and often enough where the damage done to their brain–as well as other parts of their body–will eventually become detrimental. 

While conducting her research, Dr. Hoffman assessed the effects of two drugs– aniracetam and JNJ-55511118– on the self-administration behaviors of mice in her lab. JNJ-55511118 was chosen specifically as “a potential method for medicinally managing chronic repetitive drinking associated with AUD”. She found that mice who were given aniracetam showed an increase in self-administration behaviors, whilst mice who were given JNJ-5551118 showed a decrease in the self-administration behaviors–a hopeful result that could have significant impacts on those who suffer from regulating their chronic alcohol usage behaviors. 

Harvard Health, of Harvard Medical School, posits twelve ways that people struggling with weaning off alcohol can “curb their drinking”. Some of their methods include making a list of the benefits that can stem from laying off the alcohol, keeping the living quarters free of alcoholic beverages, and considering non-alcoholic substitutes. The practicality of these methods is something that makes the idea of becoming less reliant on alcohol a more tangible, realistic goal. They also place an emphasis on asking for help when you feel that the drinking habits are becoming more problematic, avoid situations where you might be influenced by peer pressure, and don’t let a few setbacks or give-ins to temptation completely offset your goal to slow down the drinking. The process of rehabilitation is almost never linear, and it comes with many hardships, an abundance of patience, and stamina, but–coupled with JNJ-55511118–the methods suggested by Harvard Health have the potential to aid individuals with AUDs in their struggle to overcome their addictions.

References:

Hoffman, J. L.; Faccidomo, S.; Saunders, B. L.; Taylor, S. M.; Kim, M.; Hodge, C. W. Inhibition of AMPA Receptors (AMPARs) Containing Transmembrane AMPAR Regulatory Protein Γ‐8 with JNJ‐55511118 Shows Preclinical Efficacy in Reducing Chronic Repetitive Alcohol Self‐administration. Alcoholism Clin &amp; Exp Res 2021, 45 (7), 1424–1435. https://doi.org/10.1111/acer.14639

12 ways to curb your drinking. 2025 https://www.health.harvard.edu/healthy-aging-and-longevity/12-ways-to-curb-your-drinking

Stress and Physical Activity - Can dancing be used as a form of physical activity to reduce stress?

 In his lecture, Dr. Trevor Buhr discussed how exposure to stress can impact physical activity. Currently, about 1/4th of the global population and roughly 80% of adolescents don’t meet the recommended physical activity levels. Data has shown that about 60 to 70% of the population are likely to experience one or more psychological traumas before adulthood and there has been a correlation that those with PTSD are 3 times less likely to be physically active. 

In order to determine the relationship between stress and physical activity, Dr. Buhr’s research used rodents as models of stress-induced physical activity. Rats were exposed to varying amounts of stress through tail shocks and then given free access to exercise on wheels. Results indicated that the more tail shocks rats were exposed, the less they exercised. It is possible that neurophysiological changes in the prefrontal cortex or to dopamine contribute to this behavioral change. For example, stress can impact neurons in the striatum or change the expression of genes like Ube3a and Zeb2 which play a role in plasticity and protein degradation. 

Interestingly, while stress can lead to a lack of physical activity, more exercise has been shown to improve both stress and depression/anxiety symptoms. In a 2021 article, “ The effect of dancing interventions on depression symptoms, anxiety, and stress in adults without musculoskeletal disorders: An integrative review and meta-analysis” it was found that dancing can be used as a therapeutic way to reduce depression and anxiety symptoms. Dancing interventions, common ones include Salsa, Tango, or ballroom dance, are organized forms of dancing which focus on improving both physical health and mental wellbeing. The study explained how dancing helps emphasize creative and expressive aspects in individuals while enhancing cardiovascular health, balance, and social interactions and relationships. It was suggested that at least 150 minutes of moderate intensity dancing per week would be an effective form of exercise for adults to reduce stress. Although research about the mechanisms behind why and how dancing improves mental wellbeing and alleviates stress is on-going, the article suggests that dance helps release endorphins and related neurochemicals including adrenaline, dopamine and serotonin. Additionally, the social environment that the dancing takes place in could've also helped reduce stress among individuals while the music promoted emotional and mood regulation.

The relationship between physical activity and mental health is an important connection to research because while poor mental health can lead to physical inactivity, it’s been shown that actually doing more exercise can help improve those symptoms. Dance therapy especially could be beneficial for those struggling with mental health because it can be a way for people to connect with music, connect with other dancers, and express themselves, which can potentially help improve mental wellbeing. 

References:

Buhr, T. J., et al. (2023). The persistence of stress-induced physical inactivity in rats: an investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress. Frontiers in Behavioral Neuroscience, 17, 1169151. https://doi.org/10.3389/fnbeh.2023.1169151

Salihu, D., et al. (2021). The effect of dancing interventions on depression symptoms, anxiety, and stress in adults without musculoskeletal disorders: An integrative review and meta-analysis. Complementary Therapies in Clinical Practice, 45, 101467. https://doi.org/10.1016/j.ctcp.2021.101467

Build resilience to stress through physical activity sooner rather than later

Stress is a part of everyone's life, but when experienced constantly or in excess, it can become both mentally and physically detrimental. While some stress is beneficial to push you to do better, study for that test, and run that mile, too much stress can cause a loss of motivation and bring you down. One big factor that stress and mental health issues was found to affect is physical exercise. Because physical inactivity is the fourth leading risk for mortality, it is very important to look after yourself and start physical exercise sooner rather than later. 

In a presentation by Trevor Buhr taking about the study "The Persistence of Stress Induced Physical Inactivity in Rats" he raises the issue that nation-wide decreased amount of physical activity is leading to not only health problems with oneself but also changes to infrastructure and physical health monitors. The study used adult male mice that were exposed to different levels of stress by putting the rats is a cage with locked wheels for seven days and after introducing stress with episodes of either 0, 50, or 100 tail shocks. 36 hours after the shocks, they unlocked the wheels and gave then access for 9 weeks. The mice that were exposed to more stress shocks showed a decreased used of the wheels compared to the less or no stress mice, and this was shown continuously through the 9 weeks of access. Even though the depression like behaviors normalized within 1 week, the stress had already caused a long lasting change in the amount of physical activity. There was also a no stress run that demonstrated a higher dopamine turnover in the prefrontal cortex and equal amounts of dopamine was used in the stress and no stress mice. This was interesting because the stressed rats had less dopamine. This helped develop the understanding that stressful experiences with certain intensity can affect the brain to promote a decrease in physical activity. 

The article "Running from Stress: Neurobiological Mechanisms of Exercise-Induced Stress Resilience" (Nowacka-Chmielewska et al. 2022) shows another point of view of the relationship between physical activity and stress. This review shows how exercise can help the brain fight back to stressful experiences and become more resilient to stress by analyzing biological mechanisms where physical activity was shown to have some type of protection form changes to the brain related to stress. They found that regular everyday exercises help support neuroplasticity, which means it will help with forming new neural connections in the brain. BDNF, a protein that is involved with learning and memory, can also be increased with exercise. There were also discussions about physical activity showing better neurotransmitter system regulation. This article highlights that overall physical activity is shown to help people develop better stress resilience and long lasting stress mitigation. 

Both the studies look at the connection between stress and physical activity, but they look at two different perspectives. Buhr's study explains that increased stress can cause a decrease in physical activity whilst the review explained that a base of normal exercise can help protect from the stress itself. This introduces a cycle into the picture between motivation and stress. If an individual is to experience increased levels of stress, this could cause them to lose motivation to exercise, however, as an individual is doing less physical activity this can also affect their ability to have psychological or even biological benefits that exercise presents to help with stress later in life. There is also a connection to dopamine form Buhr's research and the effects of stress on neurotransmitter systems which both help with understanding that certain brain processes are influenced by physical activity and stress. 

Overall, these studies show that this problem is much more complicated than just telling people to exercise more so they feel better. Because of how stress impacts motivation, developing stress resilience is even harder after the stress hits. Understanding this relationship better can help us all find ways to create healthy everyday behaviors amongst the stresses of life. So before that stress hits, maybe try building that cycle of resilience to stress sooner rather than later to save yourself from the rising numbers of physical inactivity. Physical activity is important to manage stress but managing stress is also important to maintain physical activity. 

Buhr, Trevor J., et al. "The Persistence of Stress-Induced Physical Inactivity in Rats: An Investigation of Central Monoamine Neurotransmitters and Skeletal Muscle Oxidative Stress." Frontiers in Behavioral Neuroscience, vol. 17, 2023, p. 1169151, https://doi.org/10.3389/fnbeh.2023.1169151.

Nowacka-Chmielewska, M., Grabowska, K., Grabowski, M., Meybohm, P., Burek, M., & Małecki, A. (2022). Running from Stress: Neurobiological Mechanisms of Exercise-Induced Stress Resilience. International Journal of Molecular Sciences, 23(21), 13348. https://doi.org/10.3390/ijms232113348

Too Stressed to Sweat: Why Your Brain Stops Rewarding Exercise

 When the conversation of leading mortality factors come up, topics of smoking, and drinking come up. Heart attacks and cancer are talked about too. The idea of physical inactivity is overlooked, even though it happens to be the 4th leading cause of mortality. In fact, 80 percent of adolescents are unable to meet the recommended amount of physical inactivity. As a society, approaches focusing on infrastructure or health monitoring devices, and even education have been implemented however it doesn’t account for an important fact of why people are physically inactive: stress exposure.

In Dr. Trevor Buhr’s research talk, he explored this neurobiological relationship between stress exposure and physical inactivity. He highlighted that individuals with PTSD are three times less likely to be physically active and showed there was a correlation of how people with PTSD or a history with stress are overweight. His research compared the voluntary physical activity after an acclimation period of rats who were stressed (tail shocked) to non-stressed rats. The results between a 5 day acclimation period (of no activity allowed) versus an 8 day period where it was found that stress induced rats ran less. After this experiment was done, they looked at the Medium spiny neurons in the striatum to see how the brain was physically altered after the stress. The results indicated that stress alters plasticity genes like Ube3a and Zeb2 which affect AMPA receptors. Additionally, in the non stressed rats, the dopamine system indicated that running was affiliated with a reward. This system was essentially fried in the shocked rats, disassociating running with reward. In conclusion, stress transforms physical activity from a rewarding behavior to unrewarding, making rats unmotivated to run. 

A research article published in 2024 called, “Stressful Life Events and Reward Processing in Adults: Moderation by Depression and Anhedonia” tested if stress-related deficits in the brains reward system seen in animals would also occur in humans who were exposed to daily stressors (since previous work focused on lab). Life events in the past 6 months from 107 adults who were either currently depressed, past-depressed or never depressed were analyzed. Then, others rated each event in the past 6 months of the adult’s lives for how severe it was and if that stressor was independent of the individual’s control. Lastly, reward processing was measured through “probabilistic reward task,” where a singular response was rewarded 3 times as much as another. Anhedonia, reduced pleasure in things you would normally enjoy,was also measured. In currently depressed people, more uncontrollable stressors had poor reward learning(worse at picking up which behavior was rewarded). Past depressed and never depressed have no significant negative relationship. Within the depressed participants only adults with high anhedonia have that negative relationship and worse reward learning. The results indicate that depression and symptoms of anhedonia make people vulnerable to impaired reward learning after experiencing uncontrollable stressful events.

Dr. Buhr’s findings from the rat study show that having uncontrollable stress disrupts the dopamine-reward pathway in rodent brains. This can’t directly prove if this pathway occurs in the human brain and how it would look like at different human stressors. The 2024 study looks at everyday uncontrollable stressors in humans and how that impairs reward processing, directly expanding on Buhr’s conclusions. This study also shows the same diminishing of intrinsic reward that occurred in Buhr’s experiments. Additionally, the human data measured that defects in reward learning occur mostly in those who are currently experiencing high levels of anhedonia rather than those who have experienced high stressors, like the rats experiencing shocks in the past. These results combined could explain how physical inactivity after high stress weakens the brain's reward system so voluntarily doing something like exercise just stops having worth. So, when we take approaches to physical inactivity by implementing infrastructure and education, assuming people are only inactive because they are uneducated or don’t have access to workout, it undermines what could actually be occurring in people’s brains. If stress makes exercise feel unrewarding then addressing any stress-related reward disruption could potentially improve the physical inactivity epidemic we have. 

Buhr, T., Reed, C., Wee, O., Lee, J., Yuan, L., Fleshner, M., Valentine, R., & Clark, P. “The Persistence of Stress-Induced Physical Inactivity in Rats: An Investigation of Central Monoamine Neurotransmitters and Skeletal Muscle Oxidative Stress.” Frontiers in Behavioral Neuroscience. 2023. 

Min, Sung, Mazurka, Raegan, Pizzagalli, Diego A., Whitton, Alexis E., Milev, Roumen V., Bagby, R. Michael, Kennedy, Sidney H., Harkness, Kate L., Stressful Life Events and Reward Processing in Adults: Moderation by Depression and Anhedonia, Depression and Anxiety,  2024, 8853631, 13 pages,  2024. https://doi.org/10.1155/2024/8853631

The Complexities of Exercise

 In Dr. Buhr’s talk, he discussed how psychological stress can lead to long lasting effects on physical activity, decreasing it. In his experiment, the rats exposed to 100 tail shocks exhibited the greatest decrease in voluntary wheel running, with this effect persisting through the nine-week study. The researchers also examined whether stress affected the rats’ ability to run on a treadmill. Once the rats became more accustomed to the treadmill, the rats going through stress stopped running before the non-stressed rats. After imaging their brains, researchers found that there were differences in dopamine and other neurotransmitters between the groups. This suggests that stress can affect physical activity through changes in the brain systems involved in motivation and reward. 

This talk made me think of my own research in Dr. Steidl’s lab, where I study the dopamine system and its role in reward seeking behavior. Over the course of my research, I have become increasingly interested in how neural circuits influence whether an animal engages in a behavior associated with reward. To answer these kinds of questions, I usually frame it in a reward-seeking context, but Dr. Buhr’s talk made me consider how similar mechanisms might influence a behavior like exercise. This led me to wonder if changes in an animal’s neural systems involved in motivation could affect how willing it is to engage in a behavior that would otherwise be rewarding. 

To explore this idea further, I found the article “Gut microbes may affect motivation to exercise” from the NIH by Dohnalová, who investigated how gut microbiomes influenced exercise in mice. They found that gut microbes can produce molecules that activate sensory neurons and increase dopamine signaling in the ventral striatum during exercise. The researchers also depleted the mice’s gut biomes, which showed a reduced exercise performance and lower exercise-related dopamine responses. Once the dopamine signaling was reactivated, they were able to restore their exercise capacity. These findings exhibit how communication between the gut and brain can influence motivation to do physical activity. 

Although a different mechanism was discussed in Dr. Buhr’s talk, the connection between the two articles was interesting to me. From the talk, I learned that stress can produce lasting changes in physical activity, whereas the article explored how signals originating in the gut can influence dopamine signaling and exercise performance. Both of these findings show that physical activity is influenced by multiple biological processes rather than just an animal's ability to move. This could show that more research about how different experiences and physiological processes might affect the brain systems involved in motivation. 

These studies made me rethink how I approach inactivity in daily life. It made me recognize the complexity and nuance in assuming that someone who struggles to exercise does not simply lack discipline or willpower, but could have a multitude of factors affecting their behavior. These findings suggest that motivation is a complex process influenced by experiences and biological systems that interact with the brain. As someone who does dopamine and reward seeking behavior, I find it fascinating that dopamine related mechanisms can contribute to different types of motivated behavior, such as exercise. Using these studies, more research can be done to find a way to directly apply these findings from mice to humans and develop better ways to encourage physical activity.

Works Cited

Buhr, Trevor J., et al. “The persistence of stress-induced physical inactivity in rats: An investigation of central monoamine neurotransmitters and skeletal muscle oxidative stress.” Frontiers in Behavioral Neuroscience, 17, 1169151. https://doi.org/10.3389/fnbeh.2023.1169151 

Dohnalová, L., Lundgren, P., Carty, J.R.E. et al. A microbiome-dependent gut–brain pathway regulates motivation for exercise. Nature 612, 739–747 (2022). https://doi.org/10.1038/s41586-022-05525-z 

Alcohol: A Threat to Memory

    Almost everyone knows someone who has a problem with alcohol. Alcohol use disorders (AUDs) are the most common substance use disorders across the United States, and they have a multitude of social and personal effects. In Dr. Jessica Hoffman’s talk titled “Alcohol, Plasticity, & Brain Vulnerability,” she explained that over 29.5 million, or nearly ten percent, of Americans have diagnosed AUDs, and more are likely undiagnosed. With such a widespread problem, research is absolutely necessary to assess risks and harm that could come from consuming alcohol. While many know the negative impact alcohol has on organs such as the liver, the neurological effects are often overlooked. In both Dr. Jessica Hoffman’s talk and in the article titled “Eight or more drinks per week linked to signs of injury in the brain” from the American Academy of Neurology, alcohol consumption has been linked to detrimental effects on learning and memory and an increased risk of neurological degradation in the form of blood clots and tau tangles. 

In the article, “Eight or more drinks per week linked to signs of injury in the brain,” analysis of 1,781 people’s brains was compared with their reported drinking habits in life. Heavy drinkers, those who drank 8 or more alcoholic beverages per week, were 133% more likely to have brain lesions after adjusting for other risk factors. Heavy drinkers were also 41% more likely to have tau tangles, a key element in the development of Alzheimer's disease. Lesions often result from hyaline arteriolosclerosis, a condition that damages and stiffens blood vessels in the brain. These lesions are prone to causing cognitive decline and a loss of learning and memory function. Tau tangles, in their relation to Alzheimer’s, also seem to contribute heavily to memory decline. Former heavy drinkers, those who stopped drinking nearing their time of death, had impaired cognitive abilities. Though not as prevalent as the heavy drinkers, former heavy drinkers had increased odds of having lesions and tau tangles. This suggests that high alcohol consumption, even if cut out, may still affect brain function years later.

Dr. Jessica Hoffman’s research on the cross-section between Alzheimer’s development and alcohol in mice specifically studies how drinking can speed up the onset of neurological diseases, such as Alzheimer’s disease. Alzheimer’s disease is primarily linked to the build up of two key proteins, amyloid plaques and tau tangles. Although mice do not naturally develop Alzheimer’s disease, by using 3xtg mice and injecting human tau into mice brains, the researchers were able to compare the concentration of tau between mice who passively consumed alcohol and mice who did not. The 3xtg mice who drank alcohol scored consistently lower on various memory tests than their non-drinking peers and showed total tau and amyloid levels which suggests a more rapid onset of Alzheimer's-like symptoms. In the mice with injected human tau, those who consumed alcohol had significantly more phosphorylated tau, the damaging version of tau, than the non-alcohol group. 

Both of these studies demonstrate the neurological damage of drinking, particularly heavy drinking patterns. The article suggests that Dr. Hoffman’s observations of more rapid onset of neurological disease in alcohol-consuming mice models might also be true about alcohol consumption in humans. As the most common recreational drug, alcohol is not often thought of as a contributor to cognitive decline. However, both mouse models and human brain analysis has shown that these two factors are heavily linked. The adverse effects of alcohol seem to reduce the efficacy of memory systems even when alcohol consumption in the mice was relatively low. Perhaps alcohol itself is not as safe for our brains as we thought, especially as we grow and age.

Sources:

Eight or more drinks per week linked to signs of injury in the brain. (2025). ScienceDaily. https://www.sciencedaily.com/releases/2025/04/250409173113.htm 

Hoffman, J. L., Faccidomo, S., Saunders, B. L., Taylor, S. M., Kim, M., & Hodge, C. W. (2021). Inhibition of AMPA receptors (AMPARs) containing transmembrane AMPAR regulatory protein γ-8 with JNJ-55511118 shows preclinical efficacy in reducing chronic repetitive alcohol self-administration. Alcoholism, Clinical and Experimental Research, 45(7), 1424–1435. https://doi.org/10.1111/acer.14639