Moore et al. (2006) and Kellendock et. al (2006)

Both of the papers this week provided animal models of schizophrenia while using some overlapping tests to determine cognitive function of the mice. It is hard for me to really wrap my head around the translatability of these papers to schizophrenia in humans because they both don't touch on hallucinations at all. To be fair this would be reasonably impossible to make an animal model that completely translates to schizophrenia in humans, but both of these papers are claiming that they are modeling schizophrenia when neither of them touch on one of the main aspects of the disorder. Out of the two papers, I personally preferred the Moore et. al (2006) which looked into exposing rats to MAM during embryonic development and how this affects anatomical changes in the brain as well as behavioral tests later on. Moore et. al (2006) showed that exposure to MAM during development mimics many of the brain changes that are seen in patients with schizophrenia. The study then went on to show how this could be related to a symptom of schizophrenia by showing how rats exposed to MAME17 had an increased startle response as well as differences in reversal learning. The Kellendonk et. al (2006) also showed that rats exposed to overexpression of D2 receptors needed more trials in to be able to reverse learning when compared to the controls. To me it seems obvious that affecting the brain in these major ways such as overexpressing D2 receptors and changing the embryonic development of the brain will affect animal learning and reversal ability, but to relate this to schizophrenia and not something like a learning disability or developmental delay is a different story.

The Kellendonk et. al (2006) paper left me feeling disappointed and not really convinced of their animal model. Part of this feeling was due to the animal model not addressing the major parts of clinical schizophrenia, but I also felt like majority of the paper was negative results and I was waiting for the paper to present something that I found profound and compelling. It has been seen that dopamine changes are critical in clinical populations of schizophrenia, and this study showed differences in the connectivity of the striatum that may indicate symptoms of schizophrenia. However, in regards to the animal model brain changes that mimic clinical schizophrenia brain changes in both of these papers, I was left with the same "chicken and egg" dilemma. In humans are these brain changes seen in individuals that will develop schizophrenia or does schizophrenia develop first and then different brain changes occur? I think this is an important question to think about when assessing both of these models and their validity to show schizophrenia in animal populations.