Skip to main content

Addiction Models in Rats: Venniro et al. and deGuglielmo et al.

The paper by Venniro et al. aimed to examine the protective ability of social interaction on susceptibility to drug addiction in rats, specifically in the context of methamphetamine and heroin. One aspect of this paper that I found particularly interesting was that devaluing the social reward resulted in a sharp increase in drug self-administration across all rats, regardless of drug type or addiction score. Based on previous literature, I anticipated that rats with higher addiction scores would not exhibit the same preference for social interaction as rats with lower addiction scores – it was fascinating to see that this was not the case. As the authors acknowledge, when an individual is working to overcome addiction, their social environment tends to be very polarizing, with the potential to be a very positive protective factor or the very opposite. Therefore, I think it would have been interesting to see how the valence of the social interaction correlated with the rat’s preference for social self-administration or drug self-administration. Also, I am curious as to what the effect of social interaction would be on drug-dependent rats who had been exposed to the social defeat model. I am tempted to hypothesize that these rats would be more likely to choose the drug over social interaction, in the case that social interaction was associated with a deeper level of anxiety. 
I really enjoyed the second paper, by deGuglielmo et al., which demonstrated that optogenetic inactivation of CRF-dependent neurons in the amygdala can reverse addiction in alcoholic rats. Part of the reason I liked this paper so much, I think, was because their alcohol-dependent phenotype was very much rooted in neurobiology, through an examination of CeA CRF neurons recruited during alcohol withdrawal. I have found that with many rodent models (specifically when it comes to behavior), I struggle to see the translational validity to humans. However, with a model such as this in which the basis of the experimental conclusion was rooted in an examination of neural pathways, I felt that it was more convincing. I also thought it would be interesting to see if there were any neuronal ensembles that contributed to alcohol addiction in the nucleus accumbens, which is greatly implicated in addiction. It would be interesting to see if the NAc, as well as the amygdala, could be targeted for treatment of alcohol use disorder. 

Comments

Popular posts from this blog

Gut-Brain Interactions: Buffington et al, Reber et al 2016

April 13 Papers (Buffington et. al, Reber et. al) I found this week’s papers to be quite novel in that they both proposed potential treatments for neurodevelopmental or psychiatric disorders that target bacterial or microbial abnormalities and how these give rise to certain behavioral and physical symptoms associated with the disorders. I thought this was a very unusual yet interesting approach, and as I have not previously studied the gut-brain axis, these papers offered me a fresh perspective on researching psychiatric and neurodevelopmental disorders. They were also unconventional in their focus of the physical symptoms that often accompany mental disorders, as this is not something that I have seen many other papers touch upon very much. Particularly, I was surprised by the Reber et al paper’s focus on the link between psychiatric disorders and inflammation in organs other than the brain, such as the colon, and the Buffington et al paper’s description of a relationship between ...

Buffington et al. and Reber et al.: Gut-Brain Interactions

While I have not encountered a lot of gut-brain interaction literature yet. I found each paper unique and fascinating. Reber et al felt inaccessible for me. I felt like I didn’t understand what the goal of the paper really was and why they did the tests that they did. It seems like most of their relevant information got shoved into numerous supplementary figures and their behavior was quite difficult to follow. Multiple sections of their paper were supported with data found entirely in supplementary figures, which makes it difficult to follow the same conclusions. I have a few issues with the behavior they chose and because of this, I struggle to find driving conclusions from their work. I don’t understand why the CSC was not only the prior stressor but was also the acute stress condition both groups faced. To me, I feel like it would have made more sense to have the CSC be the prior stressor and then judge the effect on social behavior with maybe a three choice chamber test or te...

Buffington et al (2016) and Reber et al. (2016)

This week's articles were about the role of the gut-brain axis in neurodevelopment and stress. Reber and colleagues used a heat-killed version of the bacteria, M. vaccae, as a type of vaccine and found that administration to mouse models resulted in decreased response to chronic stress, prevented colitis related to stress, and reduced measures of anxiety. Reber et al. also used the inactivated M. vaccae in a mouse model of IBD and found that the bacteria prevented stress-induce flare-ups of colitis, but that this could be reversed by removing T cells. Buffington and colleagues instead examined the role of gut microbiota in maternal high-fat diets (MHFD) in the neurodevelopment and social behaviors of their offspring. Buffington et al. found that housing MHFD rats with the offspring of regular diet (MRD) rats prevented social deficits in their offspring. They also found that this co-housing arrangement prevented an imbalance in the gut bacteria Reber and colleagues' findings w...