A cannabinoid mechanism in relapse to cocaine seeking

Treatment of cocaine addiction is hampered by high rates of relapse even after prolonged drug abstinence. This relapse to compulsive cocaine use can be triggered by re-exposure to cocaine, by re-exposure to stimuli previously associated with cocaine or by exposure to stress. In laboratory rats, simi...

Full description

Saved in:

Bibliographic Details
Published in:	Nature medicine Vol. 7; no. 10; pp. 1151 - 1154
Main Authors:	De Vries, Taco J, Shaham, Yavin, Homberg, Judith R, Crombag, Hans, Schuurman, Karianne, Dieben, Jeanine, Vanderschuren, Louk J.M.J, Schoffelmeer, Anton N.M
Format:	Journal Article
Language:	English
Published:	United States Nature Publishing Group 01-10-2001
Subjects:	Animals Behavior Behavior, Animal Cannabinoid Receptor Modulators Cannabinoids - agonists Cannabinoids - antagonists & inhibitors Cannabinoids - metabolism Cocaine Cocaine - metabolism Cocaine - pharmacology Cocaine-Related Disorders - metabolism Disease Models, Animal Dronabinol - analogs & derivatives Dronabinol - metabolism Dronabinol - pharmacology Drug abuse Drug dosages Drug withdrawal Exposure Extinction Humans Piperidines - metabolism Piperidines - pharmacology Prevention Publishing Pyrazoles - metabolism Pyrazoles - pharmacology Rats Rats, Long-Evans Rats, Wistar Receptors, Cannabinoid Receptors, Drug - antagonists & inhibitors Receptors, Drug - metabolism Recurrence
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Treatment of cocaine addiction is hampered by high rates of relapse even after prolonged drug abstinence. This relapse to compulsive cocaine use can be triggered by re-exposure to cocaine, by re-exposure to stimuli previously associated with cocaine or by exposure to stress. In laboratory rats, similar events reinstate cocaine seeking after prolonged withdrawal periods, thus providing a model to study neuronal mechanisms underlying the relapse to cocaine. The endocannabinoid system has been implicated in a number of neuropsychiatric conditions, including drug addiction. The active ingredient of marijuana, Delta9-tetrahydrocannabinol, activates the mesolimbic dopamine (DA) reward system and has rewarding effects in preclinical models of drug abuse. We report here that the synthetic cannabinoid agonist, HU210 (ref. 13), provokes relapse to cocaine seeking after prolonged withdrawal periods. Furthermore, the selective CB1 receptor antagonist, SR141716A (ref. 14), attenuates relapse induced by re-exposure to cocaine-associated cues or cocaine itself, but not relapse induced by exposure to stress. These data reveal an important role of the cannabinoid system in the neuronal processes underlying relapse to cocaine seeking, and provide a rationale for the use of cannabinoid receptor antagonists for the prevention of relapse to cocaine use.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	1078-8956 1546-170X
DOI:	10.1038/nm1001-1151