These two papers used genetic and molecular approaches to examine behavioral symptoms of schizophrenia. I really enjoyed reading these two papers; they both used a comprehensive range of molecular, biological and behavioral techniques to support their findings. I first read the Burrows et. al paper. It was incredibly striking that environmental enrichment by altering the home cage and introducing novel stimuli was sufficient to create such differences in cognitive abilities. To me, this really demonstrates the importance of environment and genetic interaction in the development of a psychiatric illness. However, I was confused about how the researchers addressed interactions between mGlu5 and NMDA receptors; I was especially confused how enrichment was found to increase hyperactivity in KO mice exposed to MK-801, when KO mice already had a heightened baseline hyperactivity. The interactions between NMDA receptors, mGlu5 and environmental components is obviously quite complicated, so my lack of understanding may be in part due to this factor.
I also really enjoyed reading the Ayhan et. al paper and was excited to learn more about the DISC gene, as it is implicated in several psychiatric disorders. I found it fascinating that one mutant gene could have such significant consequences on brain anatomy, like altering brain volume and ventricle size, and I found the use of Dox to be a really efficient way to regulate gene expression. I did have some complaints about the Ayhan paper; I noticed that the two behavioral tests for depression (forced swim test and tail suspension test) were extremely similar in that they both assessed behavioral despair and hopelessness. I think integrating other behavioral tests that assess other components of depressive illness (like sucrose preference, which tests for anhedonia) may have helped strengthen their claims. While I do believe that DISC is indeed implicated in mood disorders and schizophrenia, it is clear that the researchers’ animal model of mental illness is not entirely encompassing of the complexity of either kind of disorder. As last week’s papers also displayed, this paper seems to further demonstrate that an encompassing animal model of schizophrenia does not exist due to the complicated nature of the disorder and difficulty to replicate symptoms in the lab.