Involvement of mu receptors in the opioid-induced increase in the turnover of mouse brain histamine

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

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

The effects of i.c.v injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5]enkephalin (0.5 μg i.c.v.) was antagonized by naloxone (0.3 μg i.c.v) but not by ICI 174,864 (5 μg i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 μg i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 μg i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 μg i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10-7 and 10-6 M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10-6 M) was blocked completely by naloxone (10-6 M) but not by tetrodotoxin (10-6 M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.

Original languageEnglish
Pages (from-to)1021-1026
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume244
Issue number3
Publication statusPublished - 1988

Fingerprint

mu Opioid Receptor
Histamine
Ala(2)-MePhe(4)-Gly(5)-enkephalin
Histamine Release
Brain
delta Opioid Receptor
Enkephalins
Naloxone
Opioid Analgesics
Pargyline
Nerve Endings
Tetrodotoxin
Hypothalamus
Ligands
Injections

ASJC Scopus subject areas

  • Pharmacology

Cite this

Involvement of mu receptors in the opioid-induced increase in the turnover of mouse brain histamine. / Itoh, Y.; Oishi, R.; Nishibori, Masahiro; Saeki, K.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 244, No. 3, 1988, p. 1021-1026.

Research output: Contribution to journalArticle

@article{d88e95dad53646a2882c45ea12278938,
title = "Involvement of mu receptors in the opioid-induced increase in the turnover of mouse brain histamine",
abstract = "The effects of i.c.v injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5]enkephalin (0.5 μg i.c.v.) was antagonized by naloxone (0.3 μg i.c.v) but not by ICI 174,864 (5 μg i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 μg i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 μg i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 μg i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10-7 and 10-6 M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10-6 M) was blocked completely by naloxone (10-6 M) but not by tetrodotoxin (10-6 M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.",
author = "Y. Itoh and R. Oishi and Masahiro Nishibori and K. Saeki",
year = "1988",
language = "English",
volume = "244",
pages = "1021--1026",
journal = "Journal of Pharmacology and Experimental Therapeutics",
issn = "0022-3565",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "3",

}

TY - JOUR

T1 - Involvement of mu receptors in the opioid-induced increase in the turnover of mouse brain histamine

AU - Itoh, Y.

AU - Oishi, R.

AU - Nishibori, Masahiro

AU - Saeki, K.

PY - 1988

Y1 - 1988

N2 - The effects of i.c.v injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5]enkephalin (0.5 μg i.c.v.) was antagonized by naloxone (0.3 μg i.c.v) but not by ICI 174,864 (5 μg i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 μg i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 μg i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 μg i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10-7 and 10-6 M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10-6 M) was blocked completely by naloxone (10-6 M) but not by tetrodotoxin (10-6 M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.

AB - The effects of i.c.v injected selective ligands for mu and delta opioid receptors on histamine (HA) turnover in the mouse brain were investigated to determine the receptor subclasses involved in the neurochemical response to opioids. HA turnover was measured by the accumulation of tele-methylhistamine, a major metabolite of brain HA, after pargyline injection (65 mg/kg i.p.). The increase in the HA turnover induced by [D-Ala2,D-Leu5]enkephalin (0.5 μg i.c.v.) was antagonized by naloxone (0.3 μg i.c.v) but not by ICI 174,864 (5 μg i.c.v.), a selective delta receptor antagonist. [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO; 0.1-0.5 μg i.c.v.), a selective mu receptor agonist, produced an increase in the HA turnover, whereas [D-Thr2-Leu5]enkephalin, Thr (0.1-1.0 μg i.c.v.), a selective delta receptor agonist, had little effect on the HA turnover. DAGO (0.1 μg i.c.v.) also increased the steady-state level of tele-methylhistamine but not that of HA. The effect of DAGO was observed in various brain regions except for the hypothalamus, and it was the most marked in the striatum. DAGO (10-7 and 10-6 M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release. The enhancement of HA release induced by DAGO (10-6 M) was blocked completely by naloxone (10-6 M) but not by tetrodotoxin (10-6 M). These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.

UR - http://www.scopus.com/inward/record.url?scp=0023873392&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023873392&partnerID=8YFLogxK

M3 - Article

VL - 244

SP - 1021

EP - 1026

JO - Journal of Pharmacology and Experimental Therapeutics

JF - Journal of Pharmacology and Experimental Therapeutics

SN - 0022-3565

IS - 3

ER -