Schizophrenia is an extremely complex disease of the brain, which is discussed in both Moore et al. and Kellendonk et al. Due to the various different brain structures involved in this disorder, it takes a lot of research and experiments to show just how complex it really is. Moore et al. tested for ataxia, PPI, orofacial dyskinesias and ambulation following amphetamine distribution, among other things. While their results support the schizophrenia model, they do not make it very clear on why they included the amphetamine experiment in their schizophrenia paper, unless I am missing something. One particular overlap I noticed between the two papers was the PPI experiment, although they used different variables which yielded different results. The Moore et al. experiment used MAM E17 (useful for schizophrenia models) to show that there is a decrease in prepulse inhibition of startle in that experimental group, whereas the Kellendonk et al. experiment showed that mice overexpressing D2 receptors (an increased activity of D2Rs has been linked to schizophrenia) showed no deficits in prepulse inhibition of startle. I found these results to be interesting, and most likely demonstrate the complexity and selectivity of schizophrenia.
I think these rodent models are relatively effective in studying schizophrenia due to obvious ethical reasons and overall difficulty in studying it in humans, but just how much of these animal models can we translate to humans? Schizophrenia involves a vast number of different symptoms such as hallucinations and delusions, which are not something researchers can study in animal models. I think these papers both do a good job supporting the schizophrenia model, but Kellendonk et al. does a more believable approach as they manipulate the D2 receptor, which is how many antipsychotics work.