This week’s topic is super exciting as I have always been interested in learning more about schizophrenia and the neural implications underlying the disorder. I thought Kellendonk’s paper was well drafted and the experiments were easy to understand and follow, but I wasn’t fully convinced with their results and how they were related to the hypothesis. I found it unusual that mice overexpressing D2 receptors in the striatum showed unaltered locomotor activity, sensorimotor gating and GAD, considering how impaired D2 activity is one of the primary factors in the diagnosis of the disorder. It made me wonder if this could possibly reflect an overestimation of its role? I was also confused about whether overexpression of these receptors at birth or developmentally is responsible for the deficits, because the result that normalizing D2 expression in adult mice could result in a more severe phenotype is quite bizarre. Lucia pointed out clinical implications of this result and I agree with her, what does it mean for patients consuming drugs to normalize their D2 levels? Does it only help them for certain symptoms and worsen the others? I also found it super cool that it might not be the overexpression of D2 alone but rather its downstream effects on D1 and its interaction with the PFC that together might be causing the working memory deficits. I wish they had expanded more on this because it would be interesting to know how that interaction works. It truly highlights how complicated this disorder is and how there’s so much more to investigate and learn about. Moore et al. did a good job at explaining in a very detailed manner as to why MAM-E17 is a better model for schizophrenia compared to past models. I’ve heard about this model in the past and know that it is commonly used so it was noteworthy to learn about why specifically this particular model exhibits symptoms more similar to those seen with the disorder.