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Pharmacol Biochem Behav. 2012 Feb;100(4):665-77. doi: 10.1016/j.pbb.2011.03.023. Epub 2011 Apr 1.

Glutamate signaling in the pathophysiology and therapy of schizophrenia.

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1
Department of Psychiatry, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Abstract

Glutamatergic neurotransmission, particularly through the N-methyl-d-aspartate (NMDA) receptor, has drawn attention for its role in the pathophysiology of schizophrenia. This paper reviews the neurodevelopmental origin and genetic susceptibility of schizophrenia relevant to NMDA neurotransmission, and discusses the relationship between NMDA hypofunction and different domains of symptom in schizophrenia as well as putative treatment modality for the disorder. A series of clinical trials and a meta-analysis which compared currently available NMDA-enhancing agents suggests that glycine, d-serine, and sarcosine are more efficacious than d-cycloserine in improving the overall psychopathology of schizophrenia without side effect or safety concern. In addition, enhancing glutamatergic neurotransmission via activating the AMPA receptor, metabotropic glutamate receptor or inhibition of d-amino acid oxidase (DAO) is also reviewed. More studies are needed to determine the NMDA vulnerability in schizophrenia and to confirm the long-term efficacy, functional outcome, and safety of these NMDA-enhancing agents in schizophrenic patients, particularly those with refractory negative and cognitive symptoms, or serious adverse effects while taking the existing antipsychotic agents.

PMID:
21463651
DOI:
10.1016/j.pbb.2011.03.023
[Indexed for MEDLINE]
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