Open AccessAttenuation of cue-induced reinstatement of nicotine seeking by URB597 through cannabinoid CB1 receptor in rats
Author(s) -
Benoît Forget,
Mihail Guranda,
Islam Gamaleddin,
Steven R. Goldberg,
Bernard Le Foll
Publication year - 2016
Publication title -
psychopharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.378
H-Index - 196
eISSN - 1432-2072
pISSN - 0033-3158
DOI - 10.1007/s00213-016-4232-y
Subject(s) - anandamide , endocannabinoid system , fatty acid amide hydrolase , cannabinoid receptor , nicotine , rimonabant , cannabinoid , pharmacology , chemistry , receptor , neuroscience , antagonist , psychology , medicine , biochemistry
The endocannabinoid system is composed of endocannabinoids (such as anandamide), their target receptors (CB1 and CB2 receptors, CB1Rs and CB2Rs), the enzymes that degrade them (fatty-acid-amide-hydrolase (FAAH) for anandamide), and an endocannabinoid transporter. FAAH inhibition has been recently identified as having a critical involvement in behaviors related to nicotine addiction and has been shown to reduce the effect of nicotine on the mesolimbic dopaminergic system via CB1R and peroxisome proliferator-activated receptor alpha (PPARα). Thus, inhibition of FAAH may represent a novel strategy for smoking cessation, but its mechanism of action on relapse to nicotine seeking is still unknown.
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