I found these papers super interesting. I liked how both touched on the DA hypothesis using different models and both of these models sought to show different aspects of the schizophrenic model. I think it's interesting that both of the papers showed different aspects of schizophrenia, but I have to wonder the relevance of these models since they all show just a snapshot of the disease. For example, the D2R over expressed model sought to only model the cognitive deficits of the disease, however this is just such a small part of the disorder that I am wondering how it's relevant. Is it merely to show that D2R overexpression causes this part of the disorder and perhaps other pathology causes the other behavioral problems?
I particularly liked the Moore paper, as I found it systematic and clear. It makes a pretty good case for the MAM-E17 model and shows clearly that this model is due to abnormal function in the frontal cortical circuits. This is consistent with aberrations seen in schizophrenic patients. The neurophysiology data was insightful as it clearly showed a dysregulation of the PFC as it “directs” information from the striatum. This, along with the behavioral data, makes a good case for this model as it shows the dysfunction of the frontal cortex and dopamine inputs to the striatum which is common in the pathology of schizophrenia. Additionally, I appreciated the broadness with which this model can be applied – it clearly showed multiple symptoms associated with schizophrenia vs. the narrow focus of the Kellendonk paper. Overall, I’m pretty sold on the MAM-E17 model.