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Venniro and deGuglielmo

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The first paper, Venniro et al (2018), explores the relationship between volitional social interaction and drug usage/addiction in rats. I thought their methodology and results quite thoroughly proved that, interestingly enough, volitional subject-controlled social interaction decreases drug self-administration in rats. The authors use the introduction to not only ground the research but to emphasis the human/clinical relevance of the findings, explaining the known relationship between social interaction and drug use in rodents, monkeys, and humans. Although I appreciate the thorough methodology used in this study and agree with the findings, I do not necessarily see the direct link to human treatment. Both addiction and social interaction are extremely sensitive and complicated processes in humans that are influenced by many other factors besides just each other. For example, genetic disposition, environment, mental health, impulsivity, introversion/extroversion, observational learning, perspective, and family influence are just a few. It truly is fascinating to see that the rats chose the social reward over drug self-administration, and that devaluing the social reward resulted in an increase in drug self-administration regardless of addiction score or drug class. However, I don’t see how this research can translate to or improve what we know about addiction in humans since social models of treatment are already used. I appreciated how the study used both male and female subjects, especially since we know for a fact there are distinct differences in addiction between sexes. Extending this study further, I would be interested in seeing how genetically predisposed or socially defeated rats – therefore, rats who are especially vulnerable and have unique relationships to the drug or social interaction – act in the same study.

The second paper, deGuglielmo et al (2019), was more neurobiology heavy and explored how the inactivation of a CRF-dependent pathway in the amygdala reverses addiction-like behaviors in alcohol-dependent rats. Although this paper was more technical and the first paper tried especially hard to explain the related clinical implications of their research, I had an easier time connecting this study to human models. I was fascinated to see that the authors were able to isolate a group of neurons related to withdrawal and alcohol-related memories and inactivate it, successfully reversing the rodent’s addictive behaviors. Perhaps this is just due to my current lack of expertise on the subject, but I would be interested in learning more about the distinction between “physical” withdrawal and “psychological” withdrawal. In other words, during withdrawal, a large part of the drive to keep drinking is to reduce somatic symptoms including sweating, vomiting, depression, and anxiety. However, there is clearly at least one, and probably many more, neuronal pathways in the amygdala directly relating to the urge to drink regardless of physical state. They mentioned this briefly in the study, but I would be interested to see how these two sides of withdrawal interact with each other, especially while optogenetically manipulating the pathway of CeA CRF neurons discussed in this paper. I would also be interested in doing this same experiment with addiction-related pathways in the nucleus accumbens. I was curious as to why this study only used male rodents since we know there is a difference in the way males and females respond to addiction and stress.

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