Abstract
The dorsolateral prefrontal cortex (dlPFC) mediates high-order cognition, and is profoundly afflicted in schizophrenia, including loss of dendritic spines from deep layer III, the microcircuits that generate persistent firing needed for working memory. Studies in monkeys show that these dendritic spines contain the molecular machinery for cAMP to magnify internal calcium release, where moderate levels sustain neuronal firing, but high levels weaken connectivity via opening nearby potassium channels. Genetic studies have linked schizophrenia risk with gain of function alterations in the Cav1.2 calcium channel encoded by CACNA1C, and a duplication in VIPR2, which increases cAMP intracellular signaling. The current research examined the localization of these key signaling proteins in layer III of the rhesus monkey dlPFC.
Published Version
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