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 γ-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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 82-93 |
| Number of pages | 12 |
| Journal | Pharmacotherapy |
| Volume | 16 |
| Issue number | 1 I |
| State | Published - Feb 1 1996 |
ASJC Scopus subject areas
- Pharmacology (medical)