A number of studies have suggested that disturbance in glutamatergic transm
ission in the cerebral cortex may underlie, or contribute to the pathophysi
ology of schizophrenia. In this study we examined expression of the postsyn
aptic density protein 95 (PSD95) mRNA in the prefrontal cortex and hippocam
pus in postmortem material from neuroleptic-treated schizophrenics and norm
al controls. PSD95 is known to bind to NMDA receptor subunits and is known
to be involved in synaptic plasticity. In situ hybridization analysis showe
d that the expression of PSD95 was significantly decreased in Brodmann area
9 of the prefrontal cortex but not in the hippocampus. These results furth
er implicate the prefrontal cortex in the pathophysiology of schizophrenia
and suggest dysfunction of NMDA receptors in the schizophrenic cortex. Neur
oReport 11:3133-3137 (C) 2000 Lippincott Williams & Wilkins.