Evidence map›Paper›PMID 27523303›Full record

ArticleNeuropharmacology2016

Orexin-1 receptor blockade suppresses compulsive-like alcohol drinking in mice.

Kelly Lei, Scott A Wegner, Ji-Hwan Yu, F Woodward Hopf

Abstract read
In one paragraph

Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. FGF21 analogue PF-05231023 on alcohol consumption and neuronal activity in the nucleus accumbens.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

4 authors.

Kelly LeiAlcohol Center for Translational Genetics, Department of Neurology, University of California at San Francisco, San Francisco, CA, USA.
Scott A WegnerAlcohol Center for Translational Genetics, Department of Neurology, University of California at San Francisco, San Francisco, CA, USA.
Ji-Hwan YuAlcohol Center for Translational Genetics, Department of Neurology, University of California at San Francisco, San Francisco, CA, USA.
F Woodward HopfAlcohol Center for Translational Genetics, Department of Neurology, University of California at San Francisco, San Francisco, CA, USA. Electronic address: Frederic.Hopf@ucsf.edu.

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
NIAAA NIH HHS P50 AA017072
6 · The paper itself

Abstract

Addiction is promoted by pathological motivation for addictive substances, and, despite extensive efforts, alcohol use disorders (AUDs) continue to extract a very high social, physical, and economic toll. Compulsive drinking of alcohol, where consumption persists even when alcohol is paired with negative consequences, is considered a particular obstacle for treating AUDs. Aversion-resistant alcohol intake in rodents, e.g. where rodents drink even when alcohol is paired with the bitter tastant quinine, has been considered to model some compulsive aspects of human alcohol consumption. However, the critical mechanisms that drive compulsive-like drinking are only beginning to be identified. The neuropeptide orexin has been linked to high motivation for cocaine, preferred foods, and alcohol. Thus, we investigated the role of orexin receptors in compulsive-like alcohol drinking, where C57BL/6 mice had 2-hr daily access to 15% alcohol with or without quinine (100 μM). We found that systemic administration of the widely used selective orexin-1 receptor (OX1R) blocker, SB-334867 (SB), significantly reduced compulsive-like consumption at doses lower than those reported to reduce quinine-free alcohol intake. The dose of 3-mg/kg SB, in particular, suppressed only compulsive-like drinking. Furthermore, SB did not reduce concurrent water intake during the alcohol drinking sessions, and did not alter saccharin + quinine consumption. In addition, the OX2R antagonist TCS-OX2-29 (3 or 10 mg/kg) did not alter intake of alcohol with or without quinine. Together, our results suggest that OX1R signaling is particularly important for promoting compulsive-like alcohol drinking, and that OX1Rs might represent a novel therapy to counteract compulsive aspects of human AUDs.

Indexed as

Alcohol DeterrentsAlcohol DrinkingAlcohol-Related DisordersAnimalsBenzoxazolesChoice BehaviorCompulsive BehaviorDose-Response Relationship, DrugIsoquinolinesMaleMice, Inbred C57BLNaphthyridinesOrexin Receptor AntagonistsOrexin ReceptorsPyridinesQuinine1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl urea1-(3,4-dihydro-6,7-dimethoxy-2(1H)-isoquinolinyl)-3,3-dimethyl-2-((4-pyridinylmethyl)amino)-1-butanoneAlcohol DeterrentsBenzoxazolesIsoquinolinesNaphthyridinesOrexin Receptor AntagonistsOrexin ReceptorsPyridinesQuinineUreaAlcoholCompulsiveOrexinSB-334867

Identifiers

PMID27523303
PMCPMC5065938

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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.