Kellendonk and Moore

These articles discussed two potential animal models for schizophrenia, because it is extremely difficult to observe symptoms in animals. Moore et. al (2006) used methylazoxymethanol acetate exposure to animals in embryonic day 17, while Kellendonk et. al (2006) believed that D2 receptor overexpression could produce the cognitive symptoms of schizophrenia. I found both papers fairly convincing, though they each had their own limitations and have likely been studied further in the decade since they’ve been published.

My main criticism of Kellendonk et. al (2006) is that they largely focused only on dopamine in the striatum and prefrontal cortex. Given both papers, I was not convinced that dopamine receptor expression could be considered the sole mechanism to provide a proper model of schizophrenia. I think, based on what was in the paper and what I’ve learned in other classes, that this method can only be a part of developing an animal model of schizophrenia, especially because only some symptoms are affected by current antipsychotics and thus are not the only factor in play.

I enjoyed the Moore et. al (2006) paper, in particular the thoroughness of the tests and the range of regions that were observed. I think the fact that so many regions of the brain were significantly affected by the MAM E17 treatment made this paper much more convincing. The cortical thickness/density aspects of the paper were fairly straightforward and seemed conclusive, and the spontaneous membrane activity figure showed that activity was altered when rats were exposed to MAM E17. 

Both papers were interesting and convincing, as at least part of the way to develop a schizophrenic animal model. However, I think that if the studies were to be repeated today, more tests could be done which are more advanced than the technology that was available at the time and might provide more conclusive evidence. Either way, I thought both papers were interesting and have likely been important to improving the animal model for a very complex disease.