Burrows et al described the genetic-environment interactions that could play a role in schizophrenia. Their model utilized environmental enrichment and genetic alterations in order to achieve this end. I thought this paper lacked any exciting or new information. Every test they ran seemed to be a proof of concept that had already been shown by another research team as shown by their numerous citations in the discussion portion of the paper. Furthermore, their new discoveries linking the KO of the mGlu5 to NMDA activity do not seem to have any real therapeutic usage. I feel as if they strove to prove that environmental enrichment was going to ameliorate effects of their genetic schizophrenic model when their initial model did not seem valid. Along with that, I think that environmental enrichment does not transfer over to real world experience. Mice in the wild will always be “environmentally enriched” as they are in the world or their den with many more sensory stimuli and naturally stimulating materials then standard housing in a lab could ever provide. If standard housing is supposed to model a normal everyday mouse and environmental enrichment is supposed to model an increase in these helpful developmental stimuli then I think it’s a poor paradigm. Overall their results showed that environmental enrichment alleviated some KO symptoms and showed linkage between this KO and NMDA receptors. This information while perhaps helpful for further research does not, in my opinion, have therapeutic importance as they claim.
The second paper done by Ayhan et al looked at altering a gene found to be affected in schizophrenia. This gene alteration was utilized in order to make different models for schizophrenia and see which model had similar behavioral, pharmacological, biochemical and morphological to the actual human disorder. I thought this paper was much more comprehensive than the previous, the fact that the authors went through numerous and various tests gives more validity to their models right off the bat. Their experimental manipulations of this gene were shown to cause many deficits similar to those seen in schizophrenia. Their results were often scattered and busy but the table breakdown at the end really cleared up a lot of their busy graphs. I like how they tested multiple manipulations of the gene and simply took results, then discussing the best model for schizophrenia and the role of the gene at the end of the paper. I believe the information gained in this paper and the model of gene dysfunction are good foundational work for breaking down schizophrenia.