Abstract
Heterozygous null mutations of SETD1A are definitively linked to increased schizophrenia risk in humans. Mice carrying similar mutations reportedly show deficits in spatial working memory, a cognitive function disrupted in schizophrenia. To explore the neurobiological consequences of SETD1A haploinsufficiency, we examined synchrony across neural circuits containing the medial prefrontal cortex (mPFC), nucleus reuniens (Re) of the thalamus, and ventral and dorsal hippocampus (vHPC, dHPC), four regions necessary for successful working memory performance in rodents.
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