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A Review of NMDA Receptors and the Phencyclidine Model of Schizophrenia

Sheri A. Thornberg, S. R. Saklad

Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy January 2, 1996 DOI: 10.1002/j.1875-9114.1996.tb02920.x (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Key findings Phencyclidine-induced psychosis more completely reflects the pathophysiology of schizophrenia than current models of drug-induced psychosis.

Abstract

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 7‐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.

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