Involvement of opioid receptors in phencyclidine-induced enhancement of brain histamine turnover in mice

Y. Itoh, R. Oishi, M. Nishibori, K. Saeki

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

When the histamine (HA) turnover in the brain of mice was estimated on the basis of the pargyline-induced accumulation of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, the enhancing effect of phencyclidine (PCP) on the HA turnover was antagonized by a large dose of naloxone. However, a dopamine receptor antagonist haloperidol, which is also a potent σ receptor antagonist, did not inhibit the effect of PCP on the HA turnover. [abetd-Ala2, abetd-Leu5]enkephalin, a prototypic δ opioid agonist, markedly enhanced the HA turnover. The effect of this peptide was demonstrated not only when the HA turnover was determined by the pargyline-induced t-MH accumulation but when it was estimated by the HA depletion induced by α-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. A σ agonist, SKF-10047, and a κ agonist, ethylketazocine, had no PCP-like enhancing effect on the HA turnover. These results suggest that PCP enhances the brain HA turnover in mice by stimulating, probably indireclty, endogenous opioid systems.

Original languageEnglish
Pages (from-to)285-289
Number of pages5
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume335
Issue number3
DOIs
Publication statusPublished - Mar 1987

Keywords

  • Ethylketazocine
  • Histamine turnover
  • Ketamine
  • N-Allylnormetazocine
  • [abetd-Ala,abetd-Leu]enkephalin
  • hencyclidine

ASJC Scopus subject areas

  • Pharmacology

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