title: Blocking α4β2 and α7 nicotinic acetylcholine receptors inhibits the reinstatement of morphine-induced CPP by drug priming in mice.
abstract: Investigating the interaction between nicotinic and opioid receptors is of great interest for both basic mechanistic and clinical reasons. Morphine and nicotine, two common drugs of abuse, share several behavioral and rewarding properties. However, little is known about the subtypes of nicotinic acetylcholine receptors (nAChR) in the reinstatement of morphine-induced conditioned place preference (CPP). In this study, we found that a non-specific nAChR agonist, nicotine (0.5mg/kg), had no effects on the reinstatement of morphine-induced CPP. However, we found that pretreatment with specific α(4)β(2) and α(7) nAChR subtype antagonists, dihydroxy-β-erithroidine (DHβE, 5mg/kg) and methyllycaconitine (MLA, 4 mg/kg), 20 min prior to administration of morphine, inhibited the reinstatement of morphine-induced CPP by drug priming in mice. Furthermore, depression of the reinstatement of morphine-induced CPP by a single DHβE or MLA treatment lasted at least three days later when the reinstatement was induced by morphine priming. The data suggest that specific nAChR subtypes, i.e., α(4)β(2) and α(7), may contribute to the reinstatement of morphine-induced CPP by drug priming in mice.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
authors.forename: Bin
authors.initials: B
authors.lastname: Feng
authors.forename: Jiang-hao
authors.initials: JH
authors.lastname: Xing
authors.forename: Dong
authors.initials: D
authors.lastname: Jia
authors.forename: Shui-bing
authors.initials: SB
authors.lastname: Liu
authors.forename: Hong-ju
authors.initials: HJ
authors.lastname: Guo
authors.forename: Xiao-qiang
authors.initials: XQ
authors.lastname: Li
authors.forename: Xiao-sheng
authors.initials: XS
authors.lastname: He
authors.forename: Ming-gao
authors.initials: MG
authors.lastname: Zhao
mesh_terms: D000157:Aconitine / Q000031:analogs & derivatives / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D018680:Cholinergic Antagonists / Q000494:pharmacology; D003216:Conditioning, Operant / Q000187:drug effects*; D004079:Dihydro-beta-Erythroidine / Q000494:pharmacology; D004347:Drug Interactions; D005108:Extinction, Psychological / Q000187:drug effects; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009020:Morphine / Q000008:administration & dosage*; D009043:Motor Activity / Q000187:drug effects; D009294:Narcotics / Q000008:administration & dosage*; D009538:Nicotine / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D011930:Reaction Time / Q000187:drug effects; D011978:Receptors, Nicotinic / Q000378:metabolism*; D012054:Reinforcement, Psychology; D013997:Time Factors; D064569:alpha7 Nicotinic Acetylcholine Receptor
chemical_list: D018680:Cholinergic Antagonists; C579166:Chrna7 protein, mouse; D009294:Narcotics; D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic; D064569:alpha7 Nicotinic Acetylcholine Receptor; C403531:nicotinic receptor alpha4beta2; C054634:methyllycaconitine; D004079:Dihydro-beta-Erythroidine; C004873:beta-erythroidine; D009538:Nicotine; D009020:Morphine; D000157:Aconitine