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 via Semantic Scholar
Summary
AI-generated from the abstractPhencyclidine-induced psychosis more completely reflects the pathophysiology of schizophrenia than current models of drug-induced psychosis. Phencyclidine decreases glutamatergic neurotransmission, which reduces GABA release from the nucleus accumbens, striatum, and hippocampus; may inhibit tonic dopamine release from those regions, increasing phasic dopamine reactivity; and decreases long-term potentiation. Glutamatergic system dysfunction may be involved, but pharmacologic manipulation has not revealed a clear mechanism.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Keywords | Medicine Psychology |
| Key finding | 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.