Skip to main content

Post 6

By
I was really interested to read the papers on schizophrenia animal models because schizophrenia seems to be a much more complex, internal mental illness than some of the other ones we’ve seen and its symptoms sound like they would be harder to cause and also observe in animals, especially in rodents. Some of the big symptoms that come to mind when I think of schizophrenia are hallucinations, delusions, and changes in speaking. From the little that I know about rodent research, I would imagine that these would be hard to observe in mice or rats. The Burrows (2015) paper focused on three symptoms, prepulse inhibition, long term spatial learning, and spontaneous hyperactivity. These few symptoms put together do not seem like a comprehensive representation of schizophrenia. I think this combined with my lack of background knowledge on the role NMDA plays in schizophrenia made it hard for me to fully understand how the Burrows (2015) paper really related to schizophrenia. The use of the mGLU5 receptor built off the assumption that the NMDA receptor is involved in schizophrenia. Does the NMDA receptor research that this mGLU5 receptor built off of also only use a few, unrepresentative symptoms to model schizophrenia? I could see this snowballing into a problem where research builds off of research that doesn’t fully and accurately model the illness it is supposed to model. How can scientists and journals stop this kind of domino effect?

We’ve discussed several times in class about how research has been using only male mice in experiments and leaving out female mice and we finally have a paper that uses both male and female mice in their research. It’s especially interesting that this particular research uses both male and female mice because it deals with prenatal development versus postnatal development. Male and female brains develop differently during prenatal periods and as a result are also different during postnatal development so it’s interesting to see here that there are actually differences in male and female behavior and phenotypes which support the stance that females should not be left out of research and that males are not representative of the entire species.

Comments

Post a Comment

Popular posts from this blog

Week 2- Dopamine Modulation of Depressive-like Behaviors

By
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...
Post a Comment
Read more

Sial & Allsop

By
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...
Post a Comment
Read more

Buffington and Reber

By
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...
Post a Comment
Read more