As someone who has little experience with the gut biome, it made these papers a little tricky to unpack. Reber et al had a convoluted paper that seemed to rely on the fact that those reading had preexisting knowledge of the gut biome, the effects being tested, and the desired outcomes. All of this caused many questions to arise which I will be sure to bring up in class and hopefully get answered. This paper boiled down to the fact that M. vaccae, what I understand to be a normal gut bacteria, could be utilized when killed form heat treatment as an effective method of immunoregulation. The CSC paradigm is a stress inducing model characterized by submissive gestures that the bacteria immunization attenuated at first. As the trials kept going days out however the control mice in the CSC paradigm seemed to be having fewer and fewer submissive postures whereas the bacteria treated mice kept their submissiveness equal over weeks. This occurring seems odd and was never addressed by the authors. In the same vein their elevated plus maze test which showed favorable results in the first day (the bacteria attenuating or even alieving anxiety) was even more present a week later. My problem is that the control group in this experiment should have the same results waiting 14 days till their CSC as control mice did having to wait a day until CSC right? It is the drop by almost 10% between the control groups that causes such a drastic looking effect from the immunization. Other questions came up as well and the paper kept getting more complex with their manipulations and assertions of interactions between gut biome and neuronal activity as the paper went on. I suppose I will just have to wait for class to clear up my views on this paper.
In stark contrast to Reber et al, Buffington et al utilized what felt like simple manipulations to target a specific aspect of the gut biome-ASD interaction. The video clearly laid out many of their manipulations and made reading the corresponding paper much easier. I liked how they clearly and simply showed that their high fat content treated mice had social impairments and then rescued these mice with the introduction of a bacterium thus showing at the very least an association. The drawback of this paper is the model of ASD however, the authors only tested for social behaviors. Many disorders show social dysfunction and it is a complex process. The authors mention that the mice show other symptoms as seen in ASD such as repetitive behaviors and anxiety although none of these were tested and were at best mentioned in a single passing sentence. Thus, it is difficult to trust that their model is displaying ASD.