Evidence map›Paper›PMID 20112009›Full record

ArticlePsychopharmacology2010

Neurokinin-1 receptors (NK1R:s), alcohol consumption, and alcohol reward in mice.

Annika Thorsell, Jesse R Schank, Erick Singley, Stephen P Hunt, Markus Heilig

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
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  7. The ventral pallidum and relapse in alcohol seeking.British journal of pharmacology · 2020
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  15. Several behavioral traits relevant for alcoholism are controlled by ɣ2 subunit containing GABANeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Genes and Alcohol Consumption: Studies with Mutant Mice.International review of neurobiology · 2016
    Review
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 2 institutions in 2 countries.

Annika ThorsellThe Laboratory of Clinical and Translational Studies, National Institute On Alcohol Abuse and Alcoholism, 10 Center Drive, 10-CRC/1-5330, Bethesda, MD 20892-1108, USA.
Jesse R Schank
Erick Singley
Stephen P Hunt
Markus Heilig
National Institute on Alcohol Abuse and Alcoholism · USUniversity College London · GB

Funding

Discovery and validation of novel targets for pharmacotherapy of alcoholismZIAAA000487 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI LOVINGER, DAVID M · 2009 to 2015
$23.6M
Intramural NIH HHS
6 · The paper itself

Abstract

rationaleReduced voluntary alcohol consumption was recently found in neurokinin-1 receptor (NK1R)-deficient (KO) mice. It remains unknown whether this reflects developmental effects or direct regulation of alcohol consumption by NK1R:s, and whether the reduced consumption reflects motivational effects.

objectiveThe objective of this study is to obtain an expanded preclinical validation of NK1R antagonism as a candidate therapeutic mechanism in alcohol use disorders.

methodsThe NK1R antagonist L-703,606 and NK1R KO mice were used in models that assess alcohol-related behaviors.

resultsL-703,606 (3-10 mg/kg i.p.) dose-dependently suppressed alcohol intake in WT C57BL/6 mice under two-bottle free choice conditions but was ineffective in NK1R KO:s, demonstrating the receptor specificity of the effect. Alcohol reward, measured as conditioned place preference for alcohol, was reduced by NK1R receptor deletion in a gene dose-dependent manner. In a model where escalation of intake is induced by repeated cycles of deprivation and access, escalation was seen in WT mice, but not in KO mice. Among behavioral phenotypes previously reported for NK1R mice on a mixed background, an analgesic-like phenotype was maintained on the C57BL/6 background used here, while KO:s and WT:s did not differ in anxiety- and depression-related behaviors.

conclusionsAcute blockade of NK1R:s mimics the effects of NKR1 gene deletion on alcohol consumption, supporting a direct rather than developmental role of the receptor in regulation of alcohol intake. Inactivation of NK1R:s critically modulates alcohol reward and escalation, two key characteristics of addiction. These data provide critical support for NK1R antagonism as a candidate mechanism for treatment of alcoholism.

Indexed as

Neurokinin-1 Receptor AntagonistsAlcohol DrinkingAnimalsBehavior, AnimalConditioning, PsychologicalDose-Response Relationship, DrugMiceMice, Inbred C57BLMice, KnockoutMotivationQuinuclidinesReceptors, Neurokinin-1RewardL 703606Neurokinin-1 Receptor AntagonistsQuinuclidinesReceptors, Neurokinin-1

Identifiers

PMID20112009
OpenAlexW2017929771

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.