I thoroughly enjoyed reading the Burrows et al paper. I found it extremely interesting that an enriched environment could enhance learning, memory, and synaptic plasticity. I also found it interesting that something as simple as environmental enrichment (EE) could ameliorate behavioral deficits associated with psychiatric disorders. According to multiple sources EE functions by upregulating the expression of NMDAR subunits. However, I was not completely convinced of the results presented in the paper.
Chronic administration of clozapine is said to ameliorate the deficits associated with knockout of the mGlu5 receptor and is accompanied by an increase in NMDAR. The paper postulated that the “therapeutic effects of a positive environment” parallels the therapeutic effect seen in pharmacological treatment. I would have liked to have seen data of mice that were administered clozapine and then run through the behavioral tests. That way there could have been a direct comparison of these two forms of therapy to strengthen the idea that these two therapies parallel one another.
The researchers assume all of the effects they saw of EE are due to increased expression of NMDAR subunits. I also would have liked to see data regarding NMDAR expression to confirm that NMDAR expression was indeed upregulated. I would be much more convinced of the implications of this research had the researchers performed experiments directly measuring glutamate receptor expression.During last week’s journal club we discussed how few, if any of us, thought the two models of schizophrenia presented were lacking. This week’s set of papers also offered two new models of schizophrenia. Once again focusing on the Burrows et al paper, I felt this paper was similar to the Ayhan paper in that both papers attempted to target a specific aspect of schizophrenia, in this case, mutations in a specific receptor. (D2R vs mGlu5 respectively) In both cases I felt the researchers were successful in picking apart a specific aspect of the disorder, but overall are not “great” models of schizophrenia as a whole. Both papers attempted to target the cognitive deficits associated with the disease, but neither attempt to target the positive/negative symptoms associated with the disorder. Presently it seems like schizophrenia is an umbrella term that in theory encompasses a wide range of different disorders. It is very possible that the issue does not lie with model so much as an issue with how we classify schizophrenia in general