Ayhan et al. (2011) and Burrows et al. (2015)

Both the Ayhan et al. (2011) and Burrows et al. (2015) articles presented interesting and novel findings regarding schizophrenia. Ayhan et al. (2011) focused on varying hDISC1 gene expression in transgenic mice by altering the administration time of Dox in order to examine the behavioral and morphological effects corresponding to differential expression during neurodevelopment. Burrows et al. (2015) investigated the role of the enriched environment in impacting the glutamatergic system, specifically using manipulation of glutamate mGlu5 receptors, as relates to schizophrenic behavioral expression. 

Although the Ayhan et al. (2011) article contained an extensive amount of variables within the study, they presented the information in a very organized and comprehensive way. It was evident that constant expression pre and post natally of hDISC1 (pre+post group) experienced the greatest phenotypic effects, which didn’t seem too surprising. I was surprised that only two of the effects were seen in all three expression scenarios, namely decreased dopamine in the frontal cortex of male mice and fewer PV-positive cells. I was also surprised by the increase in immobility results from the forced swim test and tail suspension test given that the former had a postnatal expression effect while the latter had a pre+post expression effect. I would have guessed that since both relate to testing learned helplessness through immobility that they would have had the same temporal expression results. One of the most interesting aspects was the separation of male and female data. This is the first study where gender-specific differences was considered, and based on the results, it was obviously an important distinction. Elucidating the neurodevelopmental timing effects of hDISC1 expression as a model could lead to important clinical research in the future, although I’m not sure about identifying a potential schizophrenic individual pre-natally, or even postnatally prior to the emergent symptoms later in adulthood.

The Burrows et al. (2015) paper was similarly well presented, and explored the gene-environment relationship, a very important, and seemingly underinvestigated, aspect of schizophrenia. When studied in conjunction with mGlu5 KO mice, an enriched environment seemed to reverse many of the behavioral deficits. According to the study, some of the effects seen in the enriched environment group were similar to those produced by the antipsychotic clozapine, meaning environmental manipulation could be quite a significant therapeutic mechanism. That said, I was curious about how to produce the same effect in human trials. What would an “enriched environment” entail? This type of environment seems like a very subjective creation based on a particular individual, but perhaps there are elements in common across schizophrenic individuals so that this model could be useful for human applications. When compared to the Ayhan et al. (2011) article, that of Burrows et al. seems more relevant to providing substantial therapies in the future.