Gut-Brain Interactions: Buffington et al. (2016) and Reber et al. (2016)

Buffington et al. (2016) and Reber et al. (2016) present quite fascinating approaches to studying the interactions or ‘axis’ between the rodent (and human) gut and brain. As the gut is a primary route for bringing things from the environment into our body, these two studies present very clear and convincing evidence for the relevance and translatable validity of their various hypotheses. 

One of the most interesting conclusions to me from Buffington et al. was that co-housing three high-fat diet offspring with just one regular-diet offspring was enough to rescue their social behavior deficits and microbiome profiles. This is remarkable, and I would like to hear more about possible mechanisms for this transfer to actually occur. Although the article mentions that mice do eat each other’s feces to transfer microbiota, could there be a certain “threshold” or level of bacteria needed to observe this phenotype switch? That is, how many more high-fat diet mice could have been housed with this one regular-diet mouse for the same changes to have been observed? Is there an “unlimited” potential of this transfer process, or are there other considerations to be taken?

Another question I had regarding the same conclusion was about potential reciprocal effects. Again, the high-fat diet offspring were housed with a regular-diet mouse in order to reverse deficits in the high-fat offspring. However, is it possible for the experimental set-up to be altered where the regular-diet mice become negatively impacted? In other words, instead of regular-diet mice helping the deficient mice regain bacteria, could the high-fat diet mice actually induce negative changes in the other and take away some of their bacteria to match the microbiome of the high-fat diet mice? I don’t know if there is a paradigm where this could be observed, but I am mostly wondering if there is always a beneficial/positive outcome from fecal transfers or if there are scenarios where the outcomes are negative, too.

A final thought on these articles relates to Reber et al. One of their primary findings was that immunized mice exposed to a chronic stressor had decreased anxiety-like behavior on the EPM, which then went on to impact gene and microglia-related observations. While I do think their conclusion is valid, it has been brought up several times this semester that the EPM can be an imperfect measure of anxiety and is also just one behavioral paradigm. I wonder if the researchers considered confirming their results with 1-2 other tests, such as the open field test or novelty suppressed feeding. For me, the additional data would have strengthened their conclusion and increased its overall credibility in the context of their other findings.