Evidence map›Paper›PMID 25451295›Full record

ArticleNeuroscience2015

Greater ethanol inhibition of presynaptic dopamine release in C57BL/6J than DBA/2J mice: Role of nicotinic acetylcholine receptors.

J T Yorgason, J H Rose, J M McIntosh, M J Ferris, S R Jones

Open access · greenAbstract readComparative Study
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Article
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  9. Dopamine Release in Nucleus Accumbens Is under Tonic Inhibition by Adenosine AThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
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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 2 institutions in 1 country.

J T YorgasonDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, United States.
J H RoseDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, United States.
J M McIntoshGeorge E. Wahlen Veterans Affairs Medical Center and Departments of Psychiatry and Biology, University of Utah, Salt Lake City, UT 84108, United States.
M J FerrisDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, United States.
S R JonesDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, United States. Electronic address: srjones@wakehealth.edu.
Wake Forest University · USUniversity of Utah · US

Funding

Venoms, Biological Resources, Molecular BiologyP01GM048677 · NIGMS · UNIVERSITY OF UTAH · PI BANDYOPADHYAY, PRADIP K · 1993 to 2018
$32.2M
BIOLOGICAL BASES OF DRUG-SEEKING BEHAVIORT32DA007262 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, JOHN T · 1991 to 2022
$9.4M
Role of Kappa Opioid Receptors in Maladaptive Catecholamine Responses to Stress and Alcohol ExposureU01AA014091 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Katherine Mercedes Holleran, SARA RAULERSON JONES · 2003 to 2026
$7.7M
Translational Studies on Early-life Stress and Vulnerability to Alcohol AddictionP01AA021099 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI WEINER, JEFFREY L. · 2012 to 2016
$2.8M
Novel nAChR-Targeted PeptidesR01GM103801 · NIGMS · UNIVERSITY OF UTAH · PI MCINTOSH, J MICHAEL · 2012 to 2019
$2.4M
nAChR Sensitivity and Individual Differences in Drug Abuse VulnerabilityK99DA031791 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FERRIS, MARK J · 2012 to 2013
$188k
Cocaine-Induced Dopamine Transporter Changes are Reversed by AmphetamineF31DA035558 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ROSE, JAMIE HANNAH · 2013 to 2015
$112k
Effects of Isolation Rearing on Dopamine Release and ReuptakeF31AA020439 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI YORGASON, JORDAN THOMAS · 2011 to 2013
$92k
NIAAA NIH HHS F31 AA020439NIAAA NIH HHS P01 AA021099NIAAA NIH HHS U01 AA014091NIDA NIH HHS F31 DA035558NIDA NIH HHS K99 DA031791NIDA NIH HHS T32 DA007262NIGMS NIH HHS P01 GM048677NIGMS NIH HHS P01 GM48677NIGMS NIH HHS R01 GM103801
6 · The paper itself

Abstract

The mesolimbic dopamine system, originating in the ventral tegmental area (VTA) and projecting to the nucleus accumbens (NAc), has been heavily implicated in the reinforcing effects of ethanol. Recent slice voltammetry studies have shown that ethanol inhibits dopamine release selectively during high-frequency activity that elicits phasic dopamine release shown to be important for learning and reinforcement. Presently, we examined ethanol inhibition of electrically evoked NAc dopamine in two mouse strains with divergent dopamine responses to ethanol, C57BL/6 (C57) and DBA/2J (DBA) mice. Previous electrophysiology and microdialysis studies have demonstrated greater ethanol-induced VTA dopaminergic firing and NAc dopamine elevations in DBA compared to C57 mice. Additionally, DBA mice have greater ethanol responses in dopamine-related behaviors, including hyperlocomotion and conditioned place preference. Currently, we demonstrate greater sensitivity of ethanol inhibition of NAc dopamine signaling in C57 compared to DBA mice. The reduced sensitivity to ethanol inhibition in DBA mice may contribute to the overall greater ethanol-induced dopamine signaling and related behaviors observed in this strain. NAc cholinergic activity is known to potently modulate terminal dopamine release. Additionally, ethanol is known to interact with multiple aspects of nicotinic acetylcholine receptor activity. Therefore, we examined ethanol-mediated inhibition of dopamine release at two ethanol concentrations (80 and 160 mM) during bath application of the non-selective nicotinic receptor antagonist mecamylamine, as well as compounds selective for the β2-(dihydro-β-erythroidine hydrobromide; DhβE) and α6-(α-conotoxin MII [H9A; L15A]) subunit-containing receptors. Mecamylamine and DhβE decreased dopamine release and reduced ethanol's inhibitory effects on dopamine in both DBA and C57 mice. Further, α-conotoxin also reduced the dopamine release and the dopamine-inhibiting effects of ethanol at the 80 mM, but not 160 mM, concentration. These data suggest that ethanol is acting in part through nicotinic acetylcholine receptors, or downstream effectors, to reduce dopamine release during high-frequency activity.

Indexed as

AnimalsCentral Nervous System DepressantsDopamineDose-Response Relationship, DrugEthanolMaleMecamylamineMice, Inbred C57BLMice, Inbred DBANicotinic AntagonistsPresynaptic TerminalsReceptors, NicotinicSpecies SpecificityTissue Culture TechniquesCentral Nervous System DepressantsDopamineEthanolMecamylamineNicotinic AntagonistsReceptors, NicotinicC57BL/6 DBA/2 miceethanol vulnerabilitymecamylaminenucleus accumbensphasic dopaminevoltammetry

Identifiers

PMID25451295
PMCPMC4274184
OpenAlexW2008747240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.