Disturbed glutamatergic neurotransmission, especially disturbed N-methyl-D-aspartate (NMDA) receptor function, has been hypothesized to be involved in the pathophysiology of schizophrenia. It may also involve abnormalities in the intracellular signaling machineries that are linked to the NMDA receptor. Postsynaptic density-95 is known to bind NMDA receptor subunits and is involved in intracellular signal transduction and synaptic plasticity. Recently, we reported that gene expression of postsynaptic density-95 was altered in schizophrenic brains compared to controls. Therefore, in this study, we examined six polymorphisms in and around the postsynaptic density-95 gene in 259 schizophrenic cases and 188 healthy controls using TaqMan technology. The results suggested that these six polymorphisms did not affect risk for schizophrenia.