While these week's papers were interesting to read, I'm not sure how much I agree with their clinical representations of schizophrenia. Beginning with the Ayhan et al. paper, I was a bit confused by their definitions of a representative model. Most noticeably, the paper kept emphasizing that their model created decreased levels of dopamine, but my understanding of schizophrenia was one of increased levels of dopamine. In addition, their was a great emphasis on the aggression found in the hDISC1 models. While aggression is a factor or symptom of schizophrenia, I don't think that a model based on aggression fully encompasses the depth and complexity of schizophrenia. I felt similarly about their tests for depression.
One thing I did like about the paper was the focus on time-dependent activation of the gene. However, if the pre and post-natal group gave symptoms that the pre-natal group didn't show, and only partially appeared for the post-natal group, how does this work? Does this mean that the gene has to be activated during the whole time to produce completely different symptoms? If so, how would varying the time frame (expanding or decreasing) alter the symptoms and increase/decrease accuracy of the model? While I believe this focus on timing is essential to moving forward in Schizophrenia research and eventually prevention, I don't think this paper really proves much in a practical setting.
The Burrows et al. paper was pretty different in that it focused on the testing of a therapeutic instead of focusing directly on the model. I found it really impressive that purely environmental factors could have an effect on behavioral symptoms. Even with the knockout, the attenuation of symptoms makes me think that this environmental enrichment would be a valid (and easy?) treatment plan to assess.