The papers this week focused on schizophrenia and dopamine, a shift from the previous weeks. Since these were the first two papers on the topic, I thought they did a good job of having enough background information on the disorder but also asked pertinent questions to further understanding of the disorder. The kellendonk et al paper wanted to address the fact that D2 receptors played an uncertain role in the activity of the PFC thus working memory and behavioral affects. The results were interesting in that their model of double transgenic mice seemed to accurately model the cognitive symptoms of schizophrenia. Under this model, it was found that D2R activity and D1R activity were not only related but their dysfunction affected one another and resulted in major cognitive deficits in these animals. The controls of this experiment were difficult since these behavioral tests loosely correspond to a specific brain activity such as spatial reasoning or sensory gating and thus it is difficult to tell if their controls accurately debunked confounds to their experiment. This was especially true when talking about the general cognitive abilities, in the transgenic mice it was said that they had cognitive impairments but not general cognitive impairments. This is a broad comparison done with just spatial reasoning (water maze) tests that did not demonstrate to me that they had all their general cognitive abilities but lacked specific ones such as working memory. Overall I thought the paper was laid out very well and used their transgenic mice intelligently to show the dysfunction of the Dopamine system and its effects on cognition in a schizophrenia model.
The next paper from Moore et al was confusing to read as the paper tried to test numerous brain areas to see the effects of this new model of schizophrenia. The entire paper seemed to center around the fact that this new model was being validated as superior to other previous models and thus the results were tests which compared the two models. These tests showed that the new model that Moore et al had made was more accurate to a schizophrenia phenotype and genotype than the previous model had been. The actual information in this paper may be used going forward as a better model of schizophrenia but with the confusing connectivity and brain regions tests it amounted to a confusing stack of scientific information that was difficult to decipher.