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• W152858918 startingPage "47" @default.
• W152858918 abstract "The glutamate hypothesis of schizophrenia has been developed based on the observation that psychotic symptoms induced by phencyclidine and related agents, which are antagonists at the N-methyl-D-aspartate (NMDA) glutamate receptor, closely resemble both the positive and negative symptoms of schizophrenia. In contrast to the dopamine hypothesis, which explains primarily with positive schizophrenic symptoms, the glutamate hypothesis may provide a more comprehensive view of the illness. Postmortem brain assays also support the glutamate hypothesis by demonstrating alterations in glutamate receptors in several brain areas in patients with schizophrenia, especially remarkable increases in the receptors in frontal and parieto-temporal association fields. This increase in glutamate receptors may reflect postsynaptic up-regulation in response to a deficiency in glutamatergic neuronal activity. Thus, the glutamate hypothesis implies that schizophrenic symptoms might be ameliorated by augmenting glutamatergic neural transmission. Recent clinical studies have been conducted using glycine, milacemide or D-cycloserine as adjuncts to or as a replacement for antipsychotics, in an attempt to augment NMDA receptor-mediated glutamatergic functions by activating the glycine modulatory site. Glycine adjuvant treatment was moderately effective in some patients in all studies and significantly improved negative symptoms in a placebo-controlled study. Replacement of antipsychotics by milacemide, a supposed glycine prodrug that crosses the blood-brain barrier, did not ameliorate schizophrenic symptoms. This lack of effect may be due to the fact that milacemide is predominantly an inhibitor of monoamine oxidases rather than a glycine agonist. Adjuvant administration of D-cycloserine, a partial agonist of the glycine site, was inconclusive, with improvement in negative symptoms occurring in one study and overall exacerbation in most patients in another study. Well designed placebo-controlled studies using orally active full agonists of the glycine regulatory site should be pursued in the future. Also, intervention at other sites within the NMDA receptor complex should be considered." @default.
• W152858918 created "2016-06-24" @default.
• W152858918 creator A5083004906 @default.
• W152858918 creator A5088324056 @default.
• W152858918 date "1997-01-01" @default.
• W152858918 modified "2023-10-14" @default.
• W152858918 title "The Glutamate Hypothesis of Schizophrenia" @default.
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