Skip to main content

Sex differences in drug abuse behavior

Holly (2012) paper

I am still a bit confused by the concept of cross-sensitization. By definition, it means the sensitization of one stimulus is generalized to a related stimulus but that it is non-associative. In this paper, I interpreted the cross-sensitization here as the sensitization of stress is generalized to the sensitization of cocaine so that stress causes the response to cocaine to be amplified and stronger (not entirely confident that’s what cross-sensitization means here). If this is what cross-sensitization refers to, I’m confused about how stress and cocaine response are related without any explicit association and why increased stress would increase the cocaine response. One thought I have is that the rewarding effects of cocaine help combat or mitigate the harmful effects of stress and so the brain adapts to stress and copes with it by amplifying any incoming rewarding stimulus. If this is the case, I wonder if other rewarding stimuli (e.g. food, sex) have similar effects when combined with stress. If being in estrous has similar neurological effects as being stressed, then it would also make sense why being in estrous also causes some longer lasting effects of cocaine.

For many of the results, I noticed that the male results were less deviated than the female results. In the 3 figures showing results for each of the 3 experiments, many of the error bars for females are larger than their male counterparts, especially those of stressed females. The male error bars are relatively small across all 3 figures. I wonder why results from male rats were more consistent with each other compared to those from female rats. Even if the wide range from females is due to small n’s, it wouldn’t explain why we don’t see this in males since the male groups had similarly low n’s.

In the introduction, I noticed that the paper uses “gender” when discussing human subjects and “sex” when discussing non-human subjects. I’m not at all familiar with human biology research. Are human subjects grouped according to their gender identity rather than their biological sex? That doesn’t make much sense since sex differences are dependent on biological sex and not gender.

Vassoler (2013)

I wonder if there would be sex differences between offspring of self-administering females the way there are sex differences between offspring of self-administering males. Females would not only contribute an egg the way males contribute sperm. Females would also gestate the offspring which would allow for more ways for the cocaine to have an impact on the offspring. However, if we could use the egg of a self-administering female and use a neutral female as a surrogate, we could investigate self-administering females’ offspring similarly to how researchers investigated self-administering males’ offspring.

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...