Skip to main content

deGuglielmo and Venniro

In deGuglielmo et al. (2019) the authors show how neuronal ensembles in the central amygdala predominantly express CRF and project to the bed nucleus of the stria terminalis. Using optogenetic dissection, they demonstrate how inactivation of this pathway reduces the dependence-related escalation of alcohol drinking and abuse. The data presented in this paper are extremely robust and point to remarkable clinical implications in binge drinking disorders. I’m also curious if a similar pathway or neural circuit is activated in drug use and dependency, and furthermore if drug-alcohol interactions cause either a change or elevation in the recruitment of a CeA neuronal ensemble. I would also like to see a study conducted using female rats, and a subsequent comparison between males and females since sexual dimorphisms have been observed in alcohol consumption and modulation. Lastly, I think a cool follow-up study could include stress as a factor, to see whether that plays a role in the intensity of somatic signs of withdrawal.

Venniro et al. (2018) takes a novel approach in using operant procedures to analyze reward competition under the assumption that unpunished and timely social interaction is preferred over drug use (meth in particular). The study also reports that social interaction has the potential to prevent incubation of drug-craving behaviors. I think the behavioral methodology that the authors employed is relevant and has definitive translational benefits. It’s been a challenge in neuroscience to study drug and alcohol dependency in rodent models since researchers often use non-drug rewards such as palatable food, a reinforcement which doesn’t really apply to humans since social rewards have a larger impact on behavior. Hence, I believe the novel paradigm used in this study promotes a greater incorporation of social reward, which can have significant translational potential for human interventions of similar nature. I also appreciated the use of both male and female rats. It would be exciting to see future developments of this model in terms of exposure to stressors such as social defeat, as well as incorporating variables such as age and maternal care.

Comments

Popular posts from this blog

Week 2- Dopamine Modulation of Depressive-like Behaviors

The Chaudhury et al paper explored the neural circuit mechanisms involved in the dopamine modulation of certain symptoms of depression. In this study, the researchers looked at social interaction and sucrose preference as part of their social-defeat paradigm, which has been shown in the past to be indicative of depressive-like behaviors. Although I initially did not completely see the connection between the social-defeat stress model of depression and the tonic vs phasic firing of dopamine neurons, it seemed that susceptibility and resilience to stress played a role in the functional/behavioral effects of dopamine firing. It was interesting to see how chronic mild stress with phasic firing of VTA dopamine neurons converted even resilient mice into susceptible mice.  The Tye et al paper similarly looked at the dopamine modulation of depressive-like behaviors, focusing on motivation with the forced swim tests and open field tests, followed by measurement of anhedonia by quantifyi...

Sial & Allsop

Sial et al. derived a novel approach for studying what they deem vicarious defeat stress (VSDS) as a model for MDD, PTSD, and other mood-related disorders as an alternative to the classical CSDS paradigm. Using adult male mice, they demonstrate that their model induces a robust and measurable social avoidant phenotype as well as other stress and anxiety related behavioral outputs. Their subsequent rescue study with chronic fluoxetine treatment shows reversal of the behavioral phenotypes and emphasizes the predictive validity of the model. Allsop et al. found that BLA-projecting ACC neurons preferentially encode socially derived aversive cue information by encoding the demonstrator’s distress response during observational learning, hence enabling acquisition of negative valence of cue by BLA neurons and behavioral output. In order to test their hypothesis, Allsop et al. used an observational fear conditional paradigm to create association between a conditioned stimulu...

Buffington and Reber

Buffington et al. explore a mechanism by which maternal obesity can induce neuronal and subsequent behavioral disorders. Using a model of high-fat diet (MHFD)-induced obesity, the authors showcase the strong connection between the brain and the gut, and its impact on behavior. The findings are provocative; by exposing these offspring to the microbiome of control offspring, there was evidence of a rescued observed behavioral phenotype. Furthermore, a phylogenetic profiling of the gut microbiome revealed a decrease in L. reuteri within MHFD offspring, and introduction of live L. reuteri into the drinking water shows successful rescue of the behavioral issues in the MHFD offspring. L. reuteri-induced expression of oxytocin within the paraventricular nuclei of the hypothalamus provides a potential mechanistic explanation for the behavioral changes. I thought this paper provided robust support for the hypothesized interaction between the gut biome and the developing CNS, with tremendous po...