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Post 10: Gut-Brain Axis

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While I am far from an expert on it, the gut-brain axis is one of the topics that is most fascinating to me in neuroscience today. Philosophers have argued for hundreds of years whether or not the body and the mind are connected, and the influence of the gut on mental health and vice versa seems to be key evidence that they are. I was excited to have the opportunity to learn more about these brain-gut interactions through Buffington et al. (2016) and Reber et al. (2016) this week, particularly in considering how the results of these experiments could point to treatments that are relatively easily translatable for humans.  

Due to my interest in the application of information about the gut-brain axis to human subjects, I put a lot of thought into what these papers may mean for the future of treatment and prevention of neurodevelopmental and anxiety disorders. Taking both papers into consideration, I wondered about the differences in the emergence of stress-related mental illnesses such as PTSD and neurodevelopmental disorders such as ASD. Both seem to be related to the gut-brain axis—PTSD being associated with deficient immunoregulation paired with stress and ASD being associated with reduced diversity of gut microbiota—but result in different disorders. This leads me to contemplate whether the specific circumstances which led to ASD- and PTSD-like phenotypes in rodents are specific to these disorders, or whether the “old friends” hypothesis can also explain the recent increase in reported ASD cases (among other reasons) and reduced microbiota diversity also puts individuals at greater risk of developing PTSD. Further, I wonder if the absence of L. reuteriis specifically associated with ASD-like behaviors and whether the absence of other species might lead to different phenotypes. 

Buffington et al. provided compelling evidence for the role of maternal obesity and gut microbiota (maternal and offspring) in offspring neurodevelopmental deficits, providing a strong base for future studies that might bring us closer to clinical applications. I would be interested in investigating the extent to which general probiotics (perhaps including L. reuteri) mimic the ameliorative effects seen with selective reintroduction of L. reuteri, if at all. I believe it would be beneficial to conduct this experiment in both mothers (fed high-fat and normal diets) as well, giving researchers more insight into whether general diversification of maternal microbiota has a protective effect for the development of neurodevelopmental disorders in offspring of obese mothers. I was also fascinated by the finding that administering MHFD offspring with oxytocin reversed their neuronal and social deficits. Given the knowledge that oxytocin production can be socially/behaviorally increased, such as through mother rats licking their offspring, I would be interested in seeing whether such maternal behaviors (or others) that increase oxytocin may have similar abilities to reverse neuronal and social deficits of MHFD offspring. It is clear that there is much more to know about the gut-brain axis, and I look forward to learning more about the topic from future research. 


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