Starting with the Kellendonk et al article, I felt as if it was a nice change from what we have been reading recently. Though there were times it was a bit wordy, the experiment was easy to follow and the results were convincing. I thought it was interesting how they used what they knew to be true in rats brains and applied it to the mice, using lesions to see if the brain areas and functions of mice were homologous to the already well-researched rats. I would be interested if they delved more into the idea that the developmental expression of D2 receptors is what causes the cognitive effects, not just the concurrent expression. What occurs during development that allows the D2 receptor expression to cause cognitive deficits? By what mechanism is this happening? Another point I found interesting was that too much or too little D1 activation leads to deficits in working memory. This shows what a complex disorder schizophrenia is and why it is so difficult to treat. I'd be curious to learn more about the optimal D1 activation in working memory and what effects too much or too little activation would have.
Moore et al was different from most of the papers we read so far, and though I found it hard to fully comprehend the details, I found the end result convincing. I've never read about the process of finding a model animal for a specific disease so I found this eye-opening. Only one point of contention I had was that I did not quite understand why the E15 rats were sporadically included throughout. I did, however, appreciate how thorough the testing was for determining the E17 to be a good model. I did not even think of how great the implications were for this until reading the final paragraph. With this more accurate model, its possible to not only test potential drugs, but actually observe the pathophysiology of the disease as it begins and progresses, something we cannot do in humans until symptoms have shown and a diagnoses has been made.