Schizoprenia animal models

The papers read for this week, both Moore et al and Kellendonk et al were trying to model schizophrenia in mice and rats, in order to understand what parts of the brain were affected.   Moore et al modeled their mice by administering MAM to prenatal animals while Kellendok et al used a D2 receptor overexpression for their schizophrenic animal model.  In addition to viewing the brain directly and observing factors such as density and neuronal counts, they used behavioral measures as to rule out other factors in addition to trying to support their findings.

Schizophrenia is a mental disorder characterized at many times by hallucinations and a person’s false beliefs therefore a huge part of diagnosis is based on the person’s reported experiences.  Consequently it was very hard for me to be completely objective or convinced by their findings, since I believe it is very hard to try to replicate what would be self reports in humans to animals that obviously can not express their feelings.  I know working with monkeys is harder, but I believe they would be a better fit for studying these measures since maybe they could falsely experience viewing letters or cues and thus express this in some test. 

I really liked that both included an introduction to what they were doing and how they were doing it, but I would have rather enjoyed for them to have a little less intro in order to dive into the study and explain what they were doing, what they found and its relevance as the paper went. 

I really liked the fact that Moore included the administration of MAM on E15 in addition to the E17, being able to support their hypothesis while contradicting previous research when showing that prenatal exposure of MAM does lead to similar behavioral and neuroanatomical characteristics of schizophrenia.  Even though, I like this paper over the Kellendrok et al paper it was harder for me to understand what they were doing.  Again, the figures were not aligned with the text.  Also, it was confusing to understand all of the different parts of the brain mentioned and keeping track of these as to better understand what should have had an effect or not.  Nonetheless, it was very convincing to have so many different measures of brain slices and its effects when administered the MAM.

One thing that really confused me was when Kellendock et al mention that “the number of D2 receptor transgenic mice reaching criteria after 28 days of training was significantly reduced compared to controls, which indicates that normalizing D2 receptor levels in chronically overexpressing adults may result in an even more severe phenotype” (Kellendock et al).  This really threw me off since I don’t understand if they are saying that if animals have this overexpression and they are treated then technically their symptoms just worsen.

Depressive and anxiety is very common in patients with schizophrenia, thus I don’t quite understand why the “schizophrenic” transgenic mice in the ___ experiment did not experience and anxiety like behavior when being put in the open maze or the open arms test.  I would expect for these to have a different experience when compared to the control. Moreover, I would also love to see if they could do a longitudinal experiment with “schizophrenic” like animal models as to observe if there are any suicidal rates as sometimes can be seen in animals and are definitely seen in schizophrenic patients.  Even though I am not an expert on tests and measures for these kinds of experiment, I understand both papers could use more modern tests to improve their research.