Glutamatergic mechanisms in schizophrenia

Schizophrenia is a chronic, severely disabling brain disorder with symptomatic onset in early adulthood. Typical antipsychotic medications that block dopamine D2 receptors are most effective in treating the psychosis but have limited effects on the negative symptoms and cognitive impairments. Consid...

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Bibliographic Details
Published in:Annual review of pharmacology and toxicology 2002-01, Vol.42 (1), p.165-179
Main Authors: Tsai, Guochuan, Coyle, Joseph T
Format: Article
Language:English
Subjects:
Animals
Dopamine - physiology
Glutamic Acid - physiology
Humans
Phencyclidine - pharmacology
Receptors, N-Methyl-D-Aspartate - drug effects
Receptors, N-Methyl-D-Aspartate - physiology
Schizophrenia - drug therapy
Schizophrenia - etiology
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Summary:Schizophrenia is a chronic, severely disabling brain disorder with symptomatic onset in early adulthood. Typical antipsychotic medications that block dopamine D2 receptors are most effective in treating the psychosis but have limited effects on the negative symptoms and cognitive impairments. Considerable research has demonstrated that noncompetitive NMDA receptor antagonists, the dissociative anaesthetic like phencyclidine and ketamine, reproduce the cardinal symptomatic features of schizophrenia. Postmortem studies reveal variable alterations in glutamate receptors and their modulators in schizophrenia. Several clinical trials indicate agents that enhance NMDA receptor function via the glycine modulatory site reduce negative and variably improve cognitive function in schizophrenics receiving typical antipsychotics. Thus, hypofunction of a subpopulation of cortico-limbic NMDA receptors may participate in the pathophysiology of schizophrenia.
ISSN:0362-1642
1545-4304
DOI:10.1146/annurev.pharmtox.42.082701.160735