title: The possible involvement of endogenous ligands for mu-, delta- and kappa-opioid receptors in modulating morphine-induced CPP expression in rats.
abstract: Previous studies suggested that electroacupuncture (EA) can suppress opioid dependence by the release of endogenous opioid peptides. To explore the site of action and the receptors involved, we tried to inject highly specific agonists for mu-, delta- and kappa-opioid receptors into the CNS to test whether it can suppress morphine-induced conditioned place preference (CPP) in the rat. Male Sprague-Dawley rats were trained with 4 mg/kg morphine, i.p. for 4 days to establish the CPP model. This CPP can be prevented by (a) i.p. injection of 3 mg/kg dose of morphine, (b) intracerebroventricular (i.c.v.) injection of micrograms doses of the selective mu-opioid receptor agonist DAMGO, delta-agonist DPDPE or kappa-agonist U-50,488H or (c) microinjection of DAMGO, DPDPE or U50488H into the shell of the nucleus accumbens (NAc). The results suggest that the release of endogenous mu-, delta- and kappa-opioid agonists in the NAc shell may play a role for EA suppression of opiate addiction.
authors.affiliation: Neuroscience Research Institute and Department of Neurobiology, Peking University Health Science Center, Key Laboratory of Neuroscience, The Ministry of Education and Ministry of Public Health, 38 Xueyuan Road, Beijing 100083, PR China.
authors.forename: Jing
authors.initials: J
authors.lastname: Liang
authors.forename: Yijing
authors.initials: Y
authors.lastname: Li
authors.forename: Xingjie
authors.initials: X
authors.lastname: Ping
authors.forename: Peng
authors.initials: P
authors.lastname: Yu
authors.forename: Yanfang
authors.initials: Y
authors.lastname: Zuo
authors.forename: Liuzhen
authors.initials: L
authors.lastname: Wu
authors.forename: Ji-Sheng
authors.initials: JS
authors.lastname: Han
authors.forename: Cailian
authors.initials: C
authors.lastname: Cui
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects* / Q000502:physiology*; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000502:physiology; D020881:Enkephalin, D-Penicillamine (2,5)- / Q000502:physiology; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D051381:Rats; D017465:Receptors, Opioid, delta / Q000819:agonists / Q000502:physiology*; D017473:Receptors, Opioid, kappa / Q000819:agonists / Q000502:physiology*; D017450:Receptors, Opioid, mu / Q000819:agonists / Q000502:physiology*
chemical_list: D017465:Receptors, Opioid, delta; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine; D020881:Enkephalin, D-Penicillamine (2,5)-