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Abstract
Neuronal communication between rodent ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC) supports cognitive functions such spatial working memory. Impaired communication between these structures underlies cognitive deficits in rodent models of predisposition to schizophrenia. Neural activity in direct vHPC-mPFC projections, as well as mPFC somatostatin-positive (SST+) interneurons, are essential for normal vHPC-mPFC communication and spatial working memory. Whether and how these two neural substrates interact to support vHPC-mPFC communication remains unclear.
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