This week's papers give insight into an emerging field in behavioral neuroscience- the role of the gut microbiome in mental health and social behaviors. Both papers acknowledge that stress can cause an imbalance in the gut microbiome, which can lead to gastrointestinal disorders and altered social behavior. However, these papers found in their own research that an existing imbalance in the gut microbiome can lead to susceptibility to stress. So which is it? This is truly a "chicken or egg" matter. To me, it appears to be a vicious cycle. Luckily, these issues can be attacked at the behavioral and gastrointestinal levels.
Buffington et al found that in their model of maternal high fat diets, reinstating only one bacterial population in the offspring was enough to relieve the neural effects of an imbalanced gut microbiome. If this were applied to humans, could a simple probiotic cocktail resolve dozens of cases of depression, autism, and other mental disorders? It seems far fetched considering that the bacterial treatment did not resolve some symptoms such as the repetitive and persevering behavior of marble burying. Then again, a little extra probiotic couldn't hurt to try. In combination with stress management techniques, could this be a new and highly efficient way to treat mental health disorders?
On a different note, I noticed one thing in the Reber et al paper of particular interest. In the "Stress Promotes Colitogenic Dysbiosis" section, they mention that beta diversity, or diversity between samples, increased with chronic subordinate colony (CSC) housing. They seem to attribute this to the effect of stress, but I thought that it would make more sense that this change in diversity across many sampled time points was actually from being exposed to different mice throughout the behavioral paradigm. Buffington et al says that families that co-habitate are known to share gut microbiota. Although the CSC housing in the Reber et al paper is hardly a loving family, isn't it possible that the mice are still sharing important gut microbiota? Furthermore, the paradigm involves changing the dominant mouse at several intervals so that the experimental mice don't habituate. Wouldn't this change introduce novel gut microbiota to their environment? And could this bring a minor beneficial effect to the experimental animals?