Skip to main content

Behavioral Sex Differences, Holly & Vassoler

Studying sex differences in response to the same stimuli is a particularly interesting topic to me. In the case of the Holly and Vassoler papers, the stimulus is cocaine. Holly et al report that cocaine binges in response to social defeat stress causes female rats to "binge" cocaine significantly more than stressed males. Also, they reported that stressed females, but not males, saw a prolonged increase of extracellular dopamine in the Nucleus Accumbens. Vassoler et al report that ingesting cocaine can have trans-generational effects on the behavior of male cocaine-users' offspring, but not female. 

Teasing apart the differences between the effects of cocaine in males and females is challenging. I think the most important thing that we can take away from the Holly and Vassoler papers is that cocaine certainly has differential effects on both sexes, both directly and trans-generationally. However, to what degree those effects are seen can vary widely depending on the organism and its environment. Are effects only seen in male offspring because the gene for "cocaine resistance" is on the Y-chromosome? The Vassoler paper mentions that progesterone has an opposing role to the effects of cocaine; could exogenous progesterone infusions prevent epigenetic changes in offspring? Further, could inhibiting progesterone in female rats who are given cocaine cause similar effects in their offspring as what's seen in the CocSired male offspring? 

Both papers show great insight into what effects cocaine have at a molecular level in the brain. Ideally, I would like to see one big study combining the methods of both papers with large cohorts of animals to see the results of every possible combination, such as the trans-generational effects of cocaine addiction under stressful conditions and the levels of dopamine in CocSired offspring. Overall, I really enjoyed reading these papers and look forward to discussing them further. 

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...