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6795946 
Journal Article 
Glutamate and schizophrenia: Beyond the dopamine hypothesis 
Coyle, JT; , 
2006 
Yes 
Cellular and Molecular Neurobiology
ISSN: 0272-4340
EISSN: 1573-6830 
SPRINGER/PLENUM PUBLISHERS 
NEW YORK 
365-384 
16773445 
WOS:000242971900006 
1. After 50 years of antipsychotic drug development focused on the dopamine D2 receptor, schizophrenia remains a chronic, disabling disorder for most affected individuals.2. Studies over the last decade demonstrate that administration of low doses of NMDA receptor antagonists can cause in normal subjects the negative symptoms, cognitive impairments and physiologic disturbances observed in schizophrenia.3. Furthermore, a number of recently identified risk genes for schizophrenia affect NMDA receptor function or glutamatergic neurotransmission.4. Placebo-controlled trials with agents that directly or indirectly activate the glycine modulatory site on the NMDA receptor have shown reduction in negative symptoms, improvement in cognition and in some cases reduction in positive symptoms in schizophrenic patients receiving concurrent antipsychotic medications.5. Thus, hypofunction of the NMDA receptor, possibly on critical GABAergic interneurons, may contribute to the pathophysiology of schizophrenia.