Linked Life Data

19679410

Source:http://linkedlifedata.com/resource/pubmed/id/19679410

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-10-19
pubmed:abstractText
Cannabinoid CB1 antagonists decrease self-administration of palatable food and several abused drugs in animals and modulate extinction of conditioned fear responses. Less is known, however, about whether and how CB1 antagonists might modulate the extinction of appetitive behavior. Therefore, this study examined the effects of the CB1 receptor antagonist rimonabant (SR141716) during extinction of responding maintained either by cocaine or by palatable foods (corn oil or Ensure), as well as responding elicited by stimulus cues that had been paired with the presentation of cocaine (i.e., cue-induced reinstatement) or a prime (presentation of cocaine or food). The effect of rimonabant on high rate responding in water-deprived mice trained to self-administer water was also examined. In mice self-administering cocaine, rimonabant attenuated cue-induced reinstatement of cocaine self-administration, the initial burst of responding during cocaine extinction and responding during spontaneous recovery. In mice self-administering corn oil, rimonabant decreased responding during extinction and also attenuated responding that had been reinstated by a priming presentation of corn oil. Moreover, mice treated with rimonabant required fewer daily sessions to reach criterion for extinction of cocaine-maintained responding than vehicle treated mice. Also, rimonabant had no effect on the rate of operant responding in mice trained to respond for water under an FR5 schedule of reinforcement. Taken together, these data suggest that in addition to attenuating the primary reinforcing effects of both palatable foods and drugs of abuse, CB1 receptor antagonism can attenuate context and cue reactivity during extinction learning and potentially enhance extinction learning in this way.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1879-0046
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
248-55
pubmed:dateRevised
2011-3-3
pubmed:meshHeading
pubmed-meshheading:19679410-Animals, pubmed-meshheading:19679410-Behavior, Addictive, pubmed-meshheading:19679410-Cocaine, pubmed-meshheading:19679410-Cocaine-Related Disorders, pubmed-meshheading:19679410-Conditioning, Operant, pubmed-meshheading:19679410-Corn Oil, pubmed-meshheading:19679410-Cues, pubmed-meshheading:19679410-Dietary Sucrose, pubmed-meshheading:19679410-Disease Models, Animal, pubmed-meshheading:19679410-Extinction, Psychological, pubmed-meshheading:19679410-Male, pubmed-meshheading:19679410-Mice, pubmed-meshheading:19679410-Mice, Inbred C57BL, pubmed-meshheading:19679410-Piperidines, pubmed-meshheading:19679410-Pyrazoles, pubmed-meshheading:19679410-Receptor, Cannabinoid, CB1, pubmed-meshheading:19679410-Recurrence, pubmed-meshheading:19679410-Reinforcement Schedule, pubmed-meshheading:19679410-Self Administration, pubmed-meshheading:19679410-Water
pubmed:year
2009
pubmed:articleTitle
The CB1 antagonist rimonabant (SR141716) blocks cue-induced reinstatement of cocaine seeking and other context and extinction phenomena predictive of relapse.
pubmed:affiliation
Temple University School of Pharmacy, 3307 North Broad Street, Philadelphia, PA 19140, United States. saraward@temple.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural