Evidence map›Paper›PMID 26864774›Full record

ArticlePsychopharmacology2016

Attenuation of cue-induced reinstatement of nicotine seeking by URB597 through cannabinoid CB1 receptor in rats.

Benoit Forget, Mihail Guranda, Islam Gamaleddin, Steven R Goldberg, Bernard Le Foll

Abstract read
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In one paragraph

Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 4 countries.

Benoit ForgetTranslational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, CAMH, 33 Russell Street, Toronto, ON, Canada, M5S 2S1.
Mihail GurandaTranslational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, CAMH, 33 Russell Street, Toronto, ON, Canada, M5S 2S1.
Islam GamaleddinTranslational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, CAMH, 33 Russell Street, Toronto, ON, Canada, M5S 2S1.
Steven R GoldbergPreclinical Pharmacology Section, Behavioral Neurosciences Branch, Intramural Research Program, NIDA, NIH, DHHS, Baltimore, MD, USA.
Bernard Le FollTranslational Addiction Research Laboratory, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, CAMH, 33 Russell Street, Toronto, ON, Canada, M5S 2S1. bernard.lefoll@camh.ca.
Centre for Addiction and Mental Health · CAInstitut Pasteur · FRUnited States Department of Health and Human Services · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleThe 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.

objectiveThe study aims to explore the mechanism of action of the inhibitor of FAAH activity, URB597, on relapse to nicotine seeking by evaluating the effect of the CB1R, CB2R, and PPARα antagonists on the attenuating effect of URB597 on cue-induced reinstatement of nicotine seeking in rats.

resultsURB597 reduced cue-induced reinstatement of nicotine seeking, an effect that was reversed by the CB1R antagonist rimonabant, but not by the CB2R or PPARα antagonists AM630 and MK886, respectively.

conclusionsThese results indicate that URB597 reduces cue-induced reinstatement in rats through a CB1 receptor-dependent mechanism, and not via CB2R or PPARα. Since FAAH inhibition represent a novel and promising strategy for tobacco smoking cessation, dissecting how it produces its action may lead to a better understanding of the neurobiological mechanisms underlying nicotine addiction.

Indexed as

AmidohydrolasesAnimalsArachidonic AcidsBenzamidesCannabinoid Receptor AntagonistsCarbamatesCuesDrug-Seeking BehaviorEndocannabinoidsFatty Acid Amide HydrolasesMaleNicotinePiperidinesPolyunsaturated AlkamidesPPAR alphaPyrazolesAmidohydrolasesanandamideArachidonic AcidsBenzamidesCannabinoid Receptor AntagonistsCarbamatescyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterEndocannabinoidsFatty Acid Amide HydrolasesNicotinePiperidinesPolyunsaturated AlkamidesPPAR alphaPyrazolesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2RimonabantIntravenous self-administrationNicotineRatsRelapseRimonabantURB597

Identifiers

PMID26864774
OpenAlexW2271641403

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.