Moore and Kellendork

Both Moore and Kellendonk worked with animal models for schizophrenia, with Moore trying to create one and Kellendonk trying to improve one. I thought it interesting the success that Moore had using MAM to create mice with a schizophrenic phenotype. Kellendonk, on the other hand, did not have the overwhelming evidence of a successful model, as they were unable to cause a significant change in locomotion, gating, or anxiety in the mice. This may be due to the fact that Kellndonk targeted D2 receptors in the prefrontal cortex, whereas Moore used MAM to affect cortex development overall. Ultimately, Kellendonk didn’t affect the actual structure of the brains like Moore did, they only altered the dopamine neurons’ activity. I say dopamine neurons, because although they targeted the D2 receptors, the D1 receptors were also affected. It was also interesting that once they stopped expressing the gene that controlled the D2 receptors, the results were still being expressed. It would be interesting to study why this occurs, and how the activation of the D2 receptors specifically alters the brain to cause this.