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Glutamatergic mechanisms in schizophrenia
Guochuan Tsai1, Joseph T Coyle
1Laboratory of Molecular and Psychiatric Neuroscience, Mailman Research Center, Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, Massachusetts 02478, USA. tsaig@helix.mgh.harvard.edu
Annual Review of Pharmacology and Toxicology
|January 25, 2002
Summary
Schizophrenia treatment may improve by targeting N-methyl-D-aspartate (NMDA) receptors. Enhancing NMDA receptor function shows promise for reducing negative symptoms and cognitive deficits in schizophrenia patients.
Area of Science:
- Neuroscience
- Psychiatry
- Pharmacology
Background:
- Schizophrenia is a chronic brain disorder impacting early adulthood.
- Current antipsychotics primarily target dopamine D2 receptors, with limited efficacy on negative symptoms and cognitive deficits.
- NMDA receptor antagonists like phencyclidine and ketamine mimic schizophrenia symptoms.
Purpose of the Study:
- To investigate the role of N-methyl-D-aspartate (NMDA) receptor hypofunction in schizophrenia pathophysiology.
- To evaluate the therapeutic potential of enhancing NMDA receptor function.
Main Methods:
- Review of postmortem studies on glutamate receptors in schizophrenia.
- Analysis of clinical trial data for agents targeting the glycine modulatory site of NMDA receptors.
Main Results:
- Postmortem studies show alterations in glutamate receptors in schizophrenia.
- Clinical trials indicate that agents enhancing NMDA receptor function via the glycine site can reduce negative symptoms.
- These agents also variably improve cognitive function in patients on typical antipsychotics.
Conclusions:
- NMDA receptor hypofunction in specific brain regions may contribute to schizophrenia.
- Targeting NMDA receptors offers a potential therapeutic strategy for schizophrenia.