Abstract
Current models of drug-induced psychosis insufficiently describe the symptoms of schizophrenia. Phencyclidine-induced psychosis is a model that more completely reflects the pathophysiology of the disease. By decreasing glutamatergic neurotransmission, phencyclidine decreases gamma-aminobutyric acid release from the nucleus accumbens, striatum, and hippocampus (manifested by MK-801); may inhibit tonic release of dopamine from the nucleus accumbens and striatum, resulting in increased dopamine phasic reactivity; and decreases long-term potentiation. Glutamatergic system dysfunction may be involved, but pharmacologic manipulation has not revealed a clear mechanism of this dysfunction.
Publication types
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Historical Article
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Review
MeSH terms
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Brain Chemistry
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Excitatory Amino Acid Antagonists / adverse effects*
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Excitatory Amino Acid Antagonists / metabolism
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History, 20th Century
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Phencyclidine / adverse effects*
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Phencyclidine / metabolism
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Psychoses, Substance-Induced* / metabolism
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Psychoses, Substance-Induced* / physiopathology
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Receptors, N-Methyl-D-Aspartate / drug effects
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Schizophrenia / chemically induced*
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Schizophrenia / metabolism
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Schizophrenia / physiopathology
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Synaptic Transmission / drug effects*
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gamma-Aminobutyric Acid / drug effects
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gamma-Aminobutyric Acid / metabolism
Substances
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Excitatory Amino Acid Antagonists
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Receptors, N-Methyl-D-Aspartate
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gamma-Aminobutyric Acid
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Phencyclidine