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What Can They Teach Us About Schizophrenia?

Arch Gen Psychiatry. 1999;56:13-17.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

IN THIS issue of the ARCHIVES, Goff et al¹ and Heresco-Levy et al² report results of clinical trials in which patients with schizophrenia were treated with D-cycloserine, a partial agonist at the glycine site on the N-methyl-D-aspartate (NMDA) subtype of glutamate (Glu) receptor, or glycine, a full agonist at the same site. As indicated by both groups, the rationale for these studies is based on the NMDA receptor hypofunction (NRHypo) hypothesis of schizophrenia. A major underpinning of this hypothesis is the observation that hypofunction of NMDA receptors induced by various NMDA antagonist drugs precipitates a transient psychotic state in healthy subjects.^3-10 Phencyclidine (PCP) and ketamine, the most extensively studied of these agents, when administered to healthy subjects, more faithfully mimic a broad range of schizophrenia-type symptoms than other psychotomimetics, including lysergic acid diethylamide (LSD) and amphetamines.^{3, 6, 8, 10} It is believed that patients with schizophrenia are unusually sensitive to pharmacological blockade . . . [Full Text of this Article]

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