The effect of phencyclidine on dopamine metabolism in the mouse brain

Kenneth M. Johnson, Kevin C. Oeffinger

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

The administration of phencyclidine (PCP) to mice resulted in no change in brain levels of tyrosine, dopamine (DA), norepinephrine (NE), or homovanillic acid (HVA). Although PCP reduced plasma tyrosine levels, no effect of PCP on the utilization of DA of NE after blockade of synthesis with α-methyl-p-tyrosine (AMPT) was observed. In addition, PCP did not affect the probenecid-induced accumulation of HVA. However, PCP was observed to potentiate the haloperidol-induced increase in HVA concentration, and the haloperidol-induced decline in DA levels after AMPT. The former effect was blocked by baclofen, suggesting that PCP mobilizes DA for impulse-dependent release. This effect could not be attributed to an antagonism of presynaptic DA receptors. These effects are similar to those of the "non-amphetamine" stimulant class of drugs.

Original languageEnglish (US)
Pages (from-to)361-369
Number of pages9
JournalLife Sciences
Volume28
Issue number4
DOIs
StatePublished - Jan 26 1981

    Fingerprint

ASJC Scopus subject areas

  • Pharmacology

Cite this