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.
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