NMDA receptor hypofunction model of schizophrenia

John W. Olney; John W. Newcomer; Nuri B. Farber

doi:10.1016/S0022-3956(99)00029-1

NMDA receptor hypofunction model of schizophrenia

John W. Olney, John W. Newcomer, Nuri B. Farber

Research output: Contribution to journal › Article › peer-review

831 Scopus citations

Abstract

Several decades of research attempting to explain schizophrenia in terms of the dopamine hyperactivity hypothesis have produced disappointing results. A new hypothesis focusing on hypofunction of the NMDA glutamate transmitter system is emerging as a potentially more promising concept. In this article, we present a version of the NMDA receptor hypofunction hypothesis that has evolved from our recent studies pertaining to the neurotoxic and psychotomimetic effects of PCP and related NMDA antagonist drugs. In this article, we examine this hypothesis in terms of its strengths and weaknesses, its therapeutic implications and ways in which it can be further tested. Copyright (C) 1999 Elsevier Science Ltd.

Original language	English
Pages (from-to)	523-533
Number of pages	11
Journal	Journal of Psychiatric Research
Volume	33
Issue number	6
DOIs	https://doi.org/10.1016/S0022-3956(99)00029-1
State	Published - 1999

Keywords

NMDA receptors
Neurodegeneration
Prevention
Psychosis
Rat model
Schizophrenia
Treatment

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10.1016/S0022-3956(99)00029-1

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title = "NMDA receptor hypofunction model of schizophrenia",

abstract = "Several decades of research attempting to explain schizophrenia in terms of the dopamine hyperactivity hypothesis have produced disappointing results. A new hypothesis focusing on hypofunction of the NMDA glutamate transmitter system is emerging as a potentially more promising concept. In this article, we present a version of the NMDA receptor hypofunction hypothesis that has evolved from our recent studies pertaining to the neurotoxic and psychotomimetic effects of PCP and related NMDA antagonist drugs. In this article, we examine this hypothesis in terms of its strengths and weaknesses, its therapeutic implications and ways in which it can be further tested. Copyright (C) 1999 Elsevier Science Ltd.",

keywords = "NMDA receptors, Neurodegeneration, Prevention, Psychosis, Rat model, Schizophrenia, Treatment",

author = "Olney, {John W.} and Newcomer, {John W.} and Farber, {Nuri B.}",

note = "Funding Information: Supported by Scientist Development Award for Clinicians DA 00290 (NBF), Independent Scientist Award MH 01510 (JWN), Research Scientist Award MH 33894 (JWO), MH 53363 (JWN), DA 05072 (JWO), AG 11355 (JWO), and NARSAD (JWN, JWO, NBF).",

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AU - Olney, John W.

AU - Newcomer, John W.

AU - Farber, Nuri B.

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AB - Several decades of research attempting to explain schizophrenia in terms of the dopamine hyperactivity hypothesis have produced disappointing results. A new hypothesis focusing on hypofunction of the NMDA glutamate transmitter system is emerging as a potentially more promising concept. In this article, we present a version of the NMDA receptor hypofunction hypothesis that has evolved from our recent studies pertaining to the neurotoxic and psychotomimetic effects of PCP and related NMDA antagonist drugs. In this article, we examine this hypothesis in terms of its strengths and weaknesses, its therapeutic implications and ways in which it can be further tested. Copyright (C) 1999 Elsevier Science Ltd.

KW - NMDA receptors

KW - Neurodegeneration

KW - Prevention

KW - Psychosis

KW - Rat model

KW - Schizophrenia

KW - Treatment

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NMDA receptor hypofunction model of schizophrenia

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