I have always thought that if one of your parents was an addict, that you were more likely to become one as well. I’m not sure if that preconceived notion was based in something scientific that I had read or if I just heard it somewhere, but I’m really happy that the Vassoler paper addressed it in the discussion. Apparently, there are data that show that cocaine addiction is heritable. Since this conflicted with their conclusion, the authors then went on to say that there are so many other aspects of addiction that could contribute to this data we see in humans. Since both genetics and environment come into play, I would really like to see them do an experiment in which they also alter the environment. I’d be curious to see if they raised the F1 generation of both cocaine sired rats and saline sired rats in a neutral environment, an enriched environment, and a negative environment. I wonder if being raised in a negative environment, with chronic stress for example, will reverse the reduced cocaine intake for cocaine sired rats. If there is an effect in this generation, do their BDNF levels also change? Is there perhaps a critical period in which this susceptibility to reduce cocaine intake can change? In regards to the Holly paper, I was surprised that females had a longer “binge” period and were more vulnerable to cocaine addiction following social defeat. I’d be really curious to see if this vulnerability also applied to chronic stress, without any social aspect. I also wonder if it’s possible to put rats on birth control. Since the estrous cycle had significant effects, I’m curious as to if artificially altering it will affect the data. I know that a lot of women take different forms of birth control and don’t get their periods. While I don’t know what exactly happens with the hormones, I’d still be curious as to if these females responded more like the males.
This weeks papers Reber et al. 2016 and Buffington et al. 2016 present a super interesting look into the gut-brain axis. Regarding both of these papers, it was amazing to see how potent favorable or unfavorable gut microbiome compositions are in affecting neuronal signaling and overall behavior. Reber et al. shows how immunoregulatory immunization with specifically heat killed M.vaccae can serve as a protective factor against chronic subordinate stress induce colotis as well as behavioral symptoms due to chronic stress as such. Interestringly, this paper depleted regulatory T cell activity via the anti CD25 antibody in order to show that the antiinflammatory mechanism induced by m vaccae immunization is depented on the secondary regulatory mechanisms offered by Treg proliferation and signaling. But, when T reg signaling was removed, this did not seem to cause a significant change in behavior . Therefore, this begs the consideration of what othe rmechanisms may be at play in order ...
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