Wednesday, March 15, 2017
actual week 6
This week’s two papers began our transition into the mental disorder of schizophrenia. Schizophrenia is not an ease disorder to study because it has so many different components that come together present as schizophrenia. Although some do not express all components of schizophrenia the main attributes include: altered brain chemistry, abnormal brain structures, and inappropriate behaviors. I read the Kellendonk et al paper first and found their approach to understanding schizophrenia my favorite. I really enjoy learning about dopaminergic pathways and I hadn’t really known that schizophrenia was characterized with a dysfunction in Dopamine 2 receptor transmission. If animal models and humans with schizophrenia have an increase in dopamine release, I felt as though we should have seen an effect on locomotion since there is an increase of dopamine in the striatum that is responsible for motor. I’m not really following how this would affect cognition and not locomotor behavior. I also had trouble following the addition of doxycycline which was supposed to normalize D2 receptors but it didn’t bring the behavior back down to control levels, it actually increased the severity of the phenotype. They also suggested that cognitive deficits were perhaps due to an imbalance in the activation of D1 receptors in the PFC, after the overexpression of D2 transmission in the striatum. I don’t understand how this imbalance can remain if they specifically shut off overexpression of D2? I understand that the brain compensates in some areas to make up for other areas not working properly, so I would assume this is what is happening in the imbalance of D1 and D2 receptors. Now that I’m writing out my thoughts on this paper, I’m not quite sure its my favorite anymore. I have a lot of questions regarding their results that I didn’t initially have when I first read through their paper. The second paper by Moore et al gave a more complete view of schizophrenia, incorporating the different components in their animal model. They tested for behavior, histopathology, and corticostriatal circuits. I think this paper was a little presumptuous stating that their animal model of using MAM-E17 rats consistently exemplified a schizophrenic model. I think more experimentation must be conducted before proclaiming such a statement. Maybe they could further study their design experiment using another animal model that isn’t as permanent as using methylazoxymethanol acetate (MAM).