I was excited to dive into a new topic outside of the realm of anxiety and depression. The first article written by Ayaan in 2011 addressed the genetic components of Schizophrenia, looking at Disrupted-In Schizophrenia-1 (DISC1)as a risk factor for schizophrenia and other psychiatric disorders. The gene expression was looked at in different stages pre, post, and both Pre + Post-natally. This article found differences in the timing of this expression as well as gender differences between male and female mice. I immediately appreciated the inclusion of two genders in this study, an approach lacking in most animal models. Many of the results regarding increased aggression were expected considering my previous knowledge of this disorder. However, I was surprised with the results regarding female mice with increase immobility in the tail suspension and forced swim tests. Given the general increased locomotion as a behavioral phenotype stereotypically associated with this disorder I found it interesting that they spent greater time immobile compared to NO mice. In addition I would be curious to learn more about why there were such stark differences here between genders. While there are several differences in the results the authors do not address them in the discussion or speculate the causality. The Ayaan article brings to the forefront the involvement of dopaminergic as well as glutamanergic neurotransmitters and systems in the pathology of schizophrenia. This notion created a good transition into reading the second article by Burrows in 2015. While this article focuses on glutaminergic receptors on a molecular level, the large take away from this study in my opinion is the effect of environmental enrichment (EE) on molecular and behavioral levels of the phenotypic expression of schizophrenia. This article takes a deep dive into the environmental component of this disorder, a topic not deeply understood especially in animal models. They were able to show that positive environmental stimuli were able to ameliorate the behaviors of a schizophrenia model. Behaviors like reduced hyperactivity and improved memory and learning were shown to directly result from an EE paradigm. In addition positive changes also occurred after treatment with clonazapam, which would be expected with anxiety like behaviors. It was exciting to read about potential improvements to treatment methods as well as a greater understanding of the environmental components of these psychological disorders.
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...
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