The NMDA receptor 'glycine modulatory site' in schizophrenia: D-serine, glycine, and beyond.

Abstract

Schizophrenia is a severe psychiatric illness that is characterized by reduced cortical connectivity, for which the underlying biological and genetic causes are not well understood. Although the currently approved antipsychotic drug treatments, which primarily modulate dopaminergic function, are effective at reducing positive symptoms (i.e. delusions and hallucinations), they do little to improve the disabling cognitive and negative (i.e. anhedonia) symptoms of patients with schizophrenia. This review details the recent genetic and neurobiological findings that link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiology of schizophrenia. It also highlights potential treatment strategies that augment NMDA receptor function to treat the synaptic deficits and cognitive impairments.

• Authors: Darrick T Balu, Joseph T Coyle
• Journal: Current opinion in pharmacology (Curr Opin Pharmacol) Vol. 20 Pg. 109-15 (Feb 2015) ISSN: 1471-4973 [Electronic] England
• PMID: 25540902 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
• Copyright: Copyright © 2014. Published by Elsevier Ltd.

Chemical References

• Antipsychotic Agents
• Receptors, N-Methyl-D-Aspartate
• Serine
• Glycine
• Dopamine

Topics

• Animals
• Antipsychotic Agents (pharmacology)
• Cognition Disorders (drug therapy, physiopathology)
• Dopamine (metabolism)
• Glycine (metabolism)
• Humans
• Receptors, N-Methyl-D-Aspartate (drug effects, metabolism)
• Schizophrenia (drug therapy, physiopathology)
• Serine (metabolism)
• Synapses (metabolism)