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Glutamate and schizophrenia: beyond the dopamine hypothesis
1Harvard Medical School, McLean Hospital, Belmont, Masschusetts 02478, USA. joseph_coyle@hms.harvard.edu
Cellular and Molecular Neurobiology
|June 15, 2006
Summary
Schizophrenia treatment may improve by targeting the N-methyl-D-aspartate (NMDA) receptor. Activating the glycine modulatory site on NMDA receptors shows promise in reducing negative and cognitive symptoms of schizophrenia.
Area of Science:
- Neuroscience
- Psychiatry
- Pharmacology
Background:
- Schizophrenia remains a chronic disorder despite 50 years of dopamine D2 receptor-focused antipsychotic development.
- Recent research implicates N-methyl-D-aspartate (NMDA) receptor hypofunction in schizophrenia pathophysiology.
- NMDA receptor antagonists can induce schizophrenia-like symptoms in healthy individuals.
Purpose of the Study:
- To explore the role of NMDA receptor hypofunction in schizophrenia.
- To evaluate the therapeutic potential of targeting the NMDA receptor for schizophrenia treatment.
Main Methods:
- Review of studies on NMDA receptor antagonists and schizophrenia symptoms.
- Analysis of genetic risk factors for schizophrenia affecting glutamatergic neurotransmission.
- Examination of placebo-controlled trials using glycine site agonists for NMDA receptors.
Main Results:
- NMDA receptor antagonists can mimic negative and cognitive symptoms of schizophrenia.
- Schizophrenia risk genes are linked to NMDA receptor function.
- Glycine site agonists on NMDA receptors reduced negative symptoms and improved cognition in patients.
Conclusions:
- NMDA receptor hypofunction, potentially in GABAergic inter-neurons, may underlie schizophrenia.
- Targeting the NMDA receptor, particularly via its glycine site, offers a promising therapeutic strategy for schizophrenia.
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