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Nicotinic acetylcholine receptors in the ventral tegmental area mediate the dopamine activating and reinforcing properties of ethanol cues.

Journal article
Authors Elin Löf
Peter Olausson
Andrea deBejczy
Rosita Stomberg
J Michael McIntosh
Jane R Taylor
Bo Söderpalm
Published in Psychopharmacology
Volume 195
Issue 3
Pages 333-43
ISSN 0033-3158
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 333-43
Language en
Links dx.doi.org/10.1007/s00213-007-0899-...
Keywords Animals, Conditioning, Operant, drug effects, Conotoxins, pharmacology, Cues, Dihydro-beta-Erythroidine, pharmacology, Dopamine, metabolism, Ethanol, pharmacology, Male, Mecamylamine, pharmacology, Microdialysis, Nicotinic Agonists, pharmacology, Nicotinic Antagonists, pharmacology, Rats, Rats, Sprague-Dawley, Rats, Wistar, Receptors, Nicotinic, physiology, Reinforcement (Psychology), Self Administration, Ventral Tegmental Area, drug effects, metabolism
Subject categories Pharmacology and Toxicology, Biological research on drug dependence, Neurobiology, Substance Abuse

Abstract

RATIONALE: Cues associated with alcohol can elicit craving, support drug-seeking and precipitate relapse. OBJECTIVES: We investigated the possible involvement of nicotinic acetylcholine receptors (nAChRs) in the ventral tegmental area (VTA) in the conditioned reinforcing properties of ethanol-associated stimuli in the rat. MATERIALS AND METHODS: First, using in vivo microdialysis, we analyzed the effect of VTA perfusion of the nonselective nAChR antagonist mecamylamine (MEC) or the selective alpha4beta2* nAChR antagonist dihydro-beta-erythroidine (DHbetaE) on the nucleus accumbens (nAc) dopaminergic response to the presentation of an ethanol-associated conditioned stimulus (CS). Second, rats were trained to associate a tone+light CS with the presentation of 10% ethanol and were subsequently tested on the acquisition of a new instrumental response with conditioned reinforcement (CR) after local VTA infusion of MEC, DHbetaE, or alpha-Conotoxin MII (alpha-CtxMII, a selective alpha3beta2* and alpha6* nAChR antagonist). RESULTS: The ethanol-associated CS elevated nAc dopamine, an effect that was blocked by VTA perfusion of MEC but not DHbetaE. Systemic administration of MEC or local VTA infusion of MEC or alpha-CtxMII selectively blocked ethanol-associated CR, whereas systemic DHbetaE had no effect. CONCLUSIONS: We hypothesize a novel mechanism by which alcohol-associated cues promote drug-seeking behavior via activation of dopamine-stimulating alpha-CtxMII-sensitive nAChRs in the VTA. Pharmacological manipulations of selective nAChRs may thus be possible treatment strategies to prevent cue-induced relapse.

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