Phencyclidine

Behavioral and biochemical evidence supporting a role for dopamine

K. M. Johnson

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

Pharmacological studies of phencyclidine (PCP)-induced behaviors such as stereotypy and turning suggest that PCP is an indirectly acting dopamine (DA) agonist with some anticholinergic potential. In vitro studies show that PCP is a potent, competitive inhibitor of monoamine uptake. PCP has also been shown to stimulate synaptosomal striatal tyrosine hydroxylase activity via a release of DA (which normally inhibits this enzyme). The mechanism by which PCP releases DA is unknown, but is similar to that of methylphenidate and distinct from that of amphetamine. In vivo studies also show similarities between PCP and the nonamphetamine class of stimulants. For example, PCP and amfonelic acid, but not amphetamine, potentiate haloperidol-induced DA metabolism. This effect can be blocked by baclofen, which suggests a dependence on nigrostriatal impulse flow. Other studies suggest that PCP releases a pool of DA that is in rapid equilibrium with the vesicular compartment, thereby activating a feedback mechanism (probably transsynaptic) that inhibits the synthesis of DA. Despite the similarities between PCP and nonamphetamine stimulants, there are both behavioral and biochemical anomalies that caution against the strict classification of PCP as a nonamphetamine stimulant.

Original languageEnglish (US)
Pages (from-to)2579-2583
Number of pages5
JournalFederation Proceedings
Volume42
Issue number9
StatePublished - 1983

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Phencyclidine
Dopamine
Pharmacology
Amphetamine
Corpus Striatum
Methylphenidate
Baclofen
Dopamine Agonists
Cholinergic Antagonists
Tyrosine 3-Monooxygenase
Haloperidol

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Phencyclidine : Behavioral and biochemical evidence supporting a role for dopamine. / Johnson, K. M.

In: Federation Proceedings, Vol. 42, No. 9, 1983, p. 2579-2583.

Research output: Contribution to journalArticle

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