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Clinical background Analysis of postmortem brains of patients with schizophrenia from the Stanley Foundation brain collection have shown consistent reduction of reelin, parvalbumin and GAD67, the 67-kilodalton isoform of glutamic acid decarboxylase, in the prefrontal cortex (PFC) and other brain regions [1]. In the PFC, this suggests a decrease in GABAergic inhibition that might be responsible for psychosis. Cognitive deficits are also a core symptom of schizophrenia, which might also be caused by GABAergic dysregulation.

Roles of prefrontal cortical GABAergic interneurons in psychosis and cognitive deficits in schizophrenia