Abstract
Schizophrenia is a severe mental illness affecting millions of people worldwide, with a substantial impact on patients, family, and society. Recent studies have established support for a hypothesis of abnormal glutamatergic neurotransmission in specific brain regions in schizophrenia involving myriad molecules associated with glutamate signaling. After a brief description of these molecules of the glutamatergic synapse, this review focuses on recent experimental evidence for glutamate abnormalities in schizophrenia, and discusses data from genetic, postmortem brain, in vivo imaging, and pharmacologic studies. These convergent findings implicate altered glutamate neurotransmission in the pathophysiology of schizophrenia, and suggest that novel therapeutic strategies targeted at modulation of glutamate neurotransmission may be useful in this illness.
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