The NMDA antagonist model for
schizophrenia: promise and pitfalls

by
Abi-Saab WM, D'Souza DC, Moghaddam B, Krystal JH
Department of Psychiatry,
Yale University School of Medicine,
New Haven, CT 06519, USA.
Pharmacopsychiatry 1998 Jul; 31 Suppl 2:104-9


ABSTRACT

Drug models have been extensively used to study the pathophysiology of schizophrenia. While they provide good insight into the neurobiology of this disorder, they have several shortcomings, which if known, help in the interpretation of results. In this paper we will discuss these shortcomings in general, and in relation to the N-methyl D-aspartate antagonist model for schizophrenia. This model has recently received a great deal of attention since both phencyclidine and the structurally related drug ketamine, produce symptoms that extend beyond psychosis per se to include other symptoms associated with schizophrenia. In fact, subanesthetic doses of ketamine in healthy individuals produce not only paranoia and perceptual alterations but also thought disorder, negative symptoms, cognitive deficits, as well as impairment on a number of electrophysiologic tests known to be abnormal in schizophrenia. These effects of ketamine will be discussed with a particular emphasis on implications for the pathophysiology and therapeutics of this disorder.
PCP
Reward
Ketamine
Glutamate
Memantine
Phencyclidine
Neuroprotectants
NMDA antagonists
Glutamate and depression
Glutamate-modulating drugs for mood disorders

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