Evidence map›Paper›PMID 26428091›Full record

ArticleBrain research bulletin2016

Exposure to nicotine increases nicotinic acetylcholine receptor density in the reward pathway and binge ethanol consumption in C57BL/6J adolescent female mice.

Alicia R Locker, Michael J Marks, Helen M Kamens, Laura Cousino Klein

Open access · greenAbstract read
In one paragraph

Article in Brain research bulletin, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Consequences of adolescent drug use.Translational psychiatry · 2023
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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 at 3 institutions in 1 country.

Alicia R LockerCenters for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV 26505, United States; The Pennsylvania State University, Department of Biobehavioral Health, University Park, PA 16802, United States. Electronic address: xzk7@cdc.gov.
Michael J MarksUniversity of Colorado Boulder, Institute for Behavioral Genetics and Department of Psychology and Neuroscience, Boulder, CO 80303, United States.
Helen M KamensThe Pennsylvania State University, Department of Biobehavioral Health, University Park, PA 16802, United States.
Laura Cousino KleinThe Pennsylvania State University, Department of Biobehavioral Health, University Park, PA 16802, United States.
Pennsylvania State University · USCenters for Disease Control and Prevention · USUniversity of Colorado Boulder · US

Funding

GENETICS OF NICOTINE TOLERANCE: ROLE OF RECEPTORSR01DA003194 · NIDA · UNIVERSITY OF COLORADO AT BOULDER · PI MARKS, MICHAEL J · 1985 to 2013
$5.5M
Genetics of Alcohol and Nicotine BehaviorsK01AA019447 · NIAAA · UNIVERSITY OF COLORADO · PI KAMENS, HELEN M · 2011 to 2015
$695k
NIAAA NIH HHS K01 AA019447NIDA NIH HHS R01 DA003194
6 · The paper itself

Abstract

Nearly 80% of adult smokers begin smoking during adolescence. Binge alcohol consumption is also common during adolescence. Past studies report that nicotine and ethanol activate dopamine neurons in the reward pathway and may increase synaptic levels of dopamine in the nucleus accumbens through nicotinic acetylcholine receptor (nAChR) stimulation. Activation of the reward pathway during adolescence through drug use may produce neural alterations affecting subsequent drug consumption. Consequently, the effect of nicotine exposure on binge alcohol consumption was examined along with an assessment of the neurobiological underpinnings that drive adolescent use of these drugs. Adolescent C57BL/6J mice (postnatal days 35-44) were exposed to either water or nicotine (200μg/ml) for ten days. On the final four days, ethanol intake was examined using the drinking-in-the-dark paradigm. Nicotine-exposed mice consumed significantly more ethanol and displayed higher blood ethanol concentrations than did control mice. Autoradiographic analysis of nAChR density revealed higher epibatidine binding in frontal cortical regions in mice exposed to nicotine and ethanol compared to mice exposed to ethanol only. These data show that nicotine exposure during adolescence increases subsequent binge ethanol consumption, and may affect the number of nAChRs in regions of the brain reward pathway, specifically the frontal cortex.

Indexed as

Alcohol DrinkingAnimalsDopamineDopaminergic NeuronsEthanolFemaleMiceMice, Inbred C57BLNicotineNicotinic AgonistsReceptors, NicotinicRewardUp-RegulationDopamineEthanolNicotineNicotinic AgonistsReceptors, NicotinicAdolescentsConsumptionEthanolMiceNicotineNicotinic acetylcholine receptors

Identifiers

PMID26428091
PMCPMC4814345
OpenAlexW2330617865

What OpenQuestion holds

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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.