A Review of NMDA Receptors and the Phencyclidine Model of Schizophrenia
Sheri A. Thornberg, S. R. Saklad
Pharmacotherapy 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.