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

I thought that both articles this week had many strengths. Ayhan et al. (2011) looked into the effects of mutant human DISC1 gene when differentially expressed at specific developmental time points. Burrows et al. (2015) looked at the effects of environmental enrichment on mice who did not have mGlu5 receptors.

Ayhan et al. (2011) was very interesting because it showed how expression of hDISC1 can affect the phenotypic features associated with many psychiatric disorders differently depending on when it is expressed during development. The inclusion of Table 1 in this paper made these differential effects very easy to understand. Another strength of this paper is that it looked at both males and females to see phenotypic differences in how hDISC1 expression caused gender-specific features. I liked that the article did this, since many psychiatric illnesses (mood disorders, schizophrenia) can present differently between genders. One question that I have about this article is, can you give humans Dox? Since we know that pre-postnatal expression of hDISC1 leads to the most significant/severe effects, it seems like -if we could test for prenatal expression of hDISC1 and then give post-natal Dox to those who expressed it prenatally, then we would be able to minimize the effects (and lessen the chance of the person developing a major psychiatric illness).

Though I thought that Ayhan et al. (2011) was a very strong paper, I preferred the Burrows et al. (2015) article. I thought that this paper had so many different strengths. First of all, the study looked at both the genetic and environmental factors associated with schizophrenia (which is important because schizophrenia is largely influenced by gene-environment interactions). Second, I thought that the study successfully showed that an enhanced environment can ameliorate the behavioral deficits caused by the mGlu5 knock-out and influence the NMDA receptor function. I really appreciated that the article showed the effects of the environment on both behavioral and biological levels. Furthermore, the paper even related the effects of a positive environment to pharmacological treatment—showing that behavioral intervention can be as powerful as medication. Third, I thought that this paper was especially strong because it provided both further insight into the role of mGlu5 in the etiology of schizophrenia, in addition to proposing a potential treatment for some of the symptoms of schizophrenia. I definitely think that this paper will impact future research into the etiology and treatment of schizophrenia. I believe that an enriched environment shows a lot of promise for some people who may have schizophrenia. However, I think that human symptoms of schizophrenia are much more complex. For example, I cannot see an enriched environment helping someone who is demonstrating many negative symptoms of schizophrenia (for instance, someone who is catatonic). I do know, from experience, that providing an enriched environment can be very therapeutic for people who are exhibiting positive symptoms of schizophrenia. Unfortunately though, it is not always possible to provide an enriched environment in a hospital setting (due to lack of funds, staff, etc.), and many people who have schizophrenia may not have what we consider an enriched environment at home.