Both papers explore the pathology of schizophrenia, with Kellendonk exploring the cause of D2 abnormalities often seen in the PFC of effected patients, and Moore uses a systems analysis to demonstrate a rat model of schizophrenia. I felt the Moore article was pretty expansive in its evidence that E17 was an effective model. I liked how the E17 rats were studied through a series of different tests from prepulse inhibition startle, oralfacial dyskensia testing, reversal learning tasks and locomotor response tasks at different ages. I find their inclusion of all these different symptoms of schizophrenia into the animal model makes it much more convincing, especially alongside of the controls. I'm interested in the historical significance of these paper as I know neuroscientists have been making great strides in both understanding schizophrenia as well as treating it and I am curious how this paper, as well as Kellendonk's have played roles in this expanding knowledge.
Kellendonk notably does not see any unaltered locomotor activity, sensorimotor gating, and generalized anxiety in his models of mice overexpressing D2 receptors. I am curious if this means a failure of Kellendonks model or evidence that D2 overexpression is more relevant to the pathology of schizophrenia effecting cognitive functioning. Moore's model does see this change in behavior as well as cognition. I also am curious what changes between mouse and rat models, specifically to schizophrenia and affected brain regions, and how do we need to think about them differently?