A review of NMDA receptors and the phencyclidine model of schizophrenia.

Current models of drug-induced psychosis insufficiently describe the symptoms of schizophrenia. Phencyclidine-induced psychosis is a model that more completely reflects the pathophysiology of the disease. By decreasing glutamatergic neurotransmission, phencyclidine decreases gamma-aminobutyric acid release from the nucleus accumbens, striatum, and hippocampus (manifested by MK-801); may inhibit tonic release of dopamine from the nucleus accumbens and striatum, resulting in increased dopamine phasic reactivity; and decreases long-term potentiation. Glutamatergic system dysfunction may be involved, but pharmacologic manipulation has not revealed a clear mechanism of this dysfunction.