α7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine

Shigeru Ishida, Yoichi Kawasaki, Hiroaki Araki, Masato Asanuma, Hisashi Matsunaga, Toshiaki Sendo, Hiromu Kawasaki, Yutaka Gomita, Yoshihisa Kitamura

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Rationale: Negative motivational withdrawal from acute opiate dependence was induced by an opioid antagonist, and the withdrawal signs prevented by pretreatment with nicotine. Objectives: The present study was undertaken to examine the mechanism of nicotine-induced attenuation of withdrawal precipitated by naloxone in rats administered a single dose of morphine. Methods: Conditioned place aversion (CPA) was precipitated by naloxone in rats exposed once to morphine. Nicotinic acetylcholine receptor (nAChR) agonists were microinjected into the central amygdaloid nucleus (CeA) before naloxone was administered. Additionally, c-Fos expression in the amygdala was measured in rats exposed to α7 nAChR ligands. Results: The microinjection of nicotine (0.3 and 1.0 μg/μl) into the CeA dose-dependently inhibited naloxone-induced CPA. This inhibition of CPA was reversed by methyllycaconitine (MLA), an α7 nAChR antagonist. CPA was also significantly attenuated by the microinjection of tropisetron (3.0 μg/μl), an α7 nAChR agonist and 5-hydroxytriptamine 3 (5-HT3) receptor antagonist, but not by ondansetron (1.0 and 3.0 μg/μl), a 5-HT3 receptor antagonist. The microinjection of PNU-282987 (3.0 μg/μl), a selective α7 nAChR agonist, into the CeA also inhibited CPA. Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus. The increase of c-Fos in the CeA was significantly inhibited by MLA. Conclusion: Nicotine-induced attenuation of CPA precipitated by naloxone is mediated by the α7 nAChR subtype, and the CeA is one of the regions of the brain involved in the effect of nicotine on acutely opiate-dependent subjects.

Original languageEnglish
Pages (from-to)923-931
Number of pages9
JournalPsychopharmacology
Volume214
Issue number4
DOIs
Publication statusPublished - Apr 2011

Fingerprint

Nicotinic Receptors
Naloxone
Nicotine
Morphine
Cholinergic Agonists
Microinjections
tropisetron
Amygdala
Opiate Alkaloids
Opioid-Related Disorders
Ondansetron
Narcotic Antagonists
Cholinergic Antagonists
Central Amygdaloid Nucleus
Ligands
Brain

Keywords

  • α7 nicotinic acetylcholine receptor
  • Acute opiate dependence
  • c-Fos
  • Central amygdaloid nucleus
  • Microinjection
  • Nicotine

ASJC Scopus subject areas

  • Pharmacology

Cite this

α7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine. / Ishida, Shigeru; Kawasaki, Yoichi; Araki, Hiroaki; Asanuma, Masato; Matsunaga, Hisashi; Sendo, Toshiaki; Kawasaki, Hiromu; Gomita, Yutaka; Kitamura, Yoshihisa.

In: Psychopharmacology, Vol. 214, No. 4, 04.2011, p. 923-931.

Research output: Contribution to journalArticle

Ishida, Shigeru ; Kawasaki, Yoichi ; Araki, Hiroaki ; Asanuma, Masato ; Matsunaga, Hisashi ; Sendo, Toshiaki ; Kawasaki, Hiromu ; Gomita, Yutaka ; Kitamura, Yoshihisa. / α7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine. In: Psychopharmacology. 2011 ; Vol. 214, No. 4. pp. 923-931.
@article{b55a17c73b9e4c8a9ff1119d29a0adfb,
title = "α7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine",
abstract = "Rationale: Negative motivational withdrawal from acute opiate dependence was induced by an opioid antagonist, and the withdrawal signs prevented by pretreatment with nicotine. Objectives: The present study was undertaken to examine the mechanism of nicotine-induced attenuation of withdrawal precipitated by naloxone in rats administered a single dose of morphine. Methods: Conditioned place aversion (CPA) was precipitated by naloxone in rats exposed once to morphine. Nicotinic acetylcholine receptor (nAChR) agonists were microinjected into the central amygdaloid nucleus (CeA) before naloxone was administered. Additionally, c-Fos expression in the amygdala was measured in rats exposed to α7 nAChR ligands. Results: The microinjection of nicotine (0.3 and 1.0 μg/μl) into the CeA dose-dependently inhibited naloxone-induced CPA. This inhibition of CPA was reversed by methyllycaconitine (MLA), an α7 nAChR antagonist. CPA was also significantly attenuated by the microinjection of tropisetron (3.0 μg/μl), an α7 nAChR agonist and 5-hydroxytriptamine 3 (5-HT3) receptor antagonist, but not by ondansetron (1.0 and 3.0 μg/μl), a 5-HT3 receptor antagonist. The microinjection of PNU-282987 (3.0 μg/μl), a selective α7 nAChR agonist, into the CeA also inhibited CPA. Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus. The increase of c-Fos in the CeA was significantly inhibited by MLA. Conclusion: Nicotine-induced attenuation of CPA precipitated by naloxone is mediated by the α7 nAChR subtype, and the CeA is one of the regions of the brain involved in the effect of nicotine on acutely opiate-dependent subjects.",
keywords = "α7 nicotinic acetylcholine receptor, Acute opiate dependence, c-Fos, Central amygdaloid nucleus, Microinjection, Nicotine",
author = "Shigeru Ishida and Yoichi Kawasaki and Hiroaki Araki and Masato Asanuma and Hisashi Matsunaga and Toshiaki Sendo and Hiromu Kawasaki and Yutaka Gomita and Yoshihisa Kitamura",
year = "2011",
month = "4",
doi = "10.1007/s00213-010-2101-7",
language = "English",
volume = "214",
pages = "923--931",
journal = "Psychopharmacology",
issn = "0033-3158",
publisher = "Springer Verlag",
number = "4",

}

TY - JOUR

T1 - α7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine

AU - Ishida, Shigeru

AU - Kawasaki, Yoichi

AU - Araki, Hiroaki

AU - Asanuma, Masato

AU - Matsunaga, Hisashi

AU - Sendo, Toshiaki

AU - Kawasaki, Hiromu

AU - Gomita, Yutaka

AU - Kitamura, Yoshihisa

PY - 2011/4

Y1 - 2011/4

N2 - Rationale: Negative motivational withdrawal from acute opiate dependence was induced by an opioid antagonist, and the withdrawal signs prevented by pretreatment with nicotine. Objectives: The present study was undertaken to examine the mechanism of nicotine-induced attenuation of withdrawal precipitated by naloxone in rats administered a single dose of morphine. Methods: Conditioned place aversion (CPA) was precipitated by naloxone in rats exposed once to morphine. Nicotinic acetylcholine receptor (nAChR) agonists were microinjected into the central amygdaloid nucleus (CeA) before naloxone was administered. Additionally, c-Fos expression in the amygdala was measured in rats exposed to α7 nAChR ligands. Results: The microinjection of nicotine (0.3 and 1.0 μg/μl) into the CeA dose-dependently inhibited naloxone-induced CPA. This inhibition of CPA was reversed by methyllycaconitine (MLA), an α7 nAChR antagonist. CPA was also significantly attenuated by the microinjection of tropisetron (3.0 μg/μl), an α7 nAChR agonist and 5-hydroxytriptamine 3 (5-HT3) receptor antagonist, but not by ondansetron (1.0 and 3.0 μg/μl), a 5-HT3 receptor antagonist. The microinjection of PNU-282987 (3.0 μg/μl), a selective α7 nAChR agonist, into the CeA also inhibited CPA. Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus. The increase of c-Fos in the CeA was significantly inhibited by MLA. Conclusion: Nicotine-induced attenuation of CPA precipitated by naloxone is mediated by the α7 nAChR subtype, and the CeA is one of the regions of the brain involved in the effect of nicotine on acutely opiate-dependent subjects.

AB - Rationale: Negative motivational withdrawal from acute opiate dependence was induced by an opioid antagonist, and the withdrawal signs prevented by pretreatment with nicotine. Objectives: The present study was undertaken to examine the mechanism of nicotine-induced attenuation of withdrawal precipitated by naloxone in rats administered a single dose of morphine. Methods: Conditioned place aversion (CPA) was precipitated by naloxone in rats exposed once to morphine. Nicotinic acetylcholine receptor (nAChR) agonists were microinjected into the central amygdaloid nucleus (CeA) before naloxone was administered. Additionally, c-Fos expression in the amygdala was measured in rats exposed to α7 nAChR ligands. Results: The microinjection of nicotine (0.3 and 1.0 μg/μl) into the CeA dose-dependently inhibited naloxone-induced CPA. This inhibition of CPA was reversed by methyllycaconitine (MLA), an α7 nAChR antagonist. CPA was also significantly attenuated by the microinjection of tropisetron (3.0 μg/μl), an α7 nAChR agonist and 5-hydroxytriptamine 3 (5-HT3) receptor antagonist, but not by ondansetron (1.0 and 3.0 μg/μl), a 5-HT3 receptor antagonist. The microinjection of PNU-282987 (3.0 μg/μl), a selective α7 nAChR agonist, into the CeA also inhibited CPA. Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus. The increase of c-Fos in the CeA was significantly inhibited by MLA. Conclusion: Nicotine-induced attenuation of CPA precipitated by naloxone is mediated by the α7 nAChR subtype, and the CeA is one of the regions of the brain involved in the effect of nicotine on acutely opiate-dependent subjects.

KW - α7 nicotinic acetylcholine receptor

KW - Acute opiate dependence

KW - c-Fos

KW - Central amygdaloid nucleus

KW - Microinjection

KW - Nicotine

UR - http://www.scopus.com/inward/record.url?scp=79953671614&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79953671614&partnerID=8YFLogxK

U2 - 10.1007/s00213-010-2101-7

DO - 10.1007/s00213-010-2101-7

M3 - Article

C2 - 21125398

AN - SCOPUS:79953671614

VL - 214

SP - 923

EP - 931

JO - Psychopharmacology

JF - Psychopharmacology

SN - 0033-3158

IS - 4

ER -