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A Review of NMDA Receptors and the Phencyclidine Model of Schizophrenia
Author(s) -
Thornberg Sheri A.,
Saklad Stephen R.
Publication year - 1996
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1996.tb02920.x
Subject(s) - phencyclidine , glutamatergic , nucleus accumbens , neuroscience , striatum , dopamine , nmda receptor , psychosis , long term potentiation , schizophrenia (object oriented programming) , medicine , psychology , glutamate receptor , pharmacology , receptor , psychiatry
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.