Both of these articles adequately demonstrate a pathological basis for schizophrenia. The Kellendonk article and the Moore article use cross-checking methods to make sure that the results they are seeing aren’t due to any additional factors. This is especially important for the Moore article because an important piece was proving that MAM utilization at E17 was more accurate in demonstrating schizophrenia than those previously administered on E15. I think that each article does a great job in experimentally showing how these pathologies influence schizophrenia-like behavior, but one thing I found interesting is that in some of the behavioral observations, these papers actually differed. For example, Moore states that there was a significant deficit in prepulse inhibition, whereas Kellendonk found “no differences in the attenuation of the response to the acoustic stimulus after the prepulse.” Moore also found that there was a significant deficit in reversal learning, where Kellendonk found “a mild deficit in reversal to the rule.” These two somewhat contrasting results make more sense when remembering that mental illnesses are extremely complex diseases with often multiple pathologies. It is extremely possible that poor development influenced by MAM could cause deficits in prepulse inhibition and reversal learning, while an increase in D2 receptors may not cause that behavioral phenotype. Both of these schizophrenic pathologies may be working together to create the complete behavioral picture of the disease. While these papers are trying to stand alone as an explanation to schizophrenia, they need to take into account other pathological findings that may occur at the same time in patients that suffer from this illness.
Another interesting finding by Kellendonk was that D2 receptors are expressed in the striatum at E17.5, which would occur after Moore administered the MAM to her E17 pups. This could also account for the differences seen between these two studies. The use of MAM did not allow for the development of D2 receptors necessary for a schizophrenic phenotype, and thus, Moore obtained results that differ than those influenced by D2 receptors.