Evidence map›Paper›PMID 22245775›Full record

ReviewPhysiology & behavior2012

The neurobiology of binge-like ethanol drinking: evidence from rodent models.

Gretchen M Sprow, Todd E Thiele

Open access · greenAbstract readReview
In one paragraph

Review in Physiology & behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 96 citations in OpenAlex.

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  8. Basolateral amygdala neuropeptide Y system modulates binge ethanol consumption.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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  20. Activation of hypothalamic oxytocin neurons reduces binge-like alcohol drinking through signaling at central oxytocin receptors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article

4 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Gretchen M SprowDepartment of Psychology, University of North Carolina, Chapel Hill, NC 27599-3270, USA.
Todd E Thiele
University of North Carolina at Chapel Hill · US

Funding

Neuropeptide Y: Role in Ethanol Intake and SensitivityR01AA013573 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI THIELE, TODD ERIC · 2001 to 2018
$3.8M
Neuropeptide Y: Role in Ethanol Intake and SensitivityR37AA013573 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TODD Eric THIELE · 2019 to 2026
$3.0M
Melanocortin Neuropeptides &Ethanol IntakeR01AA015148 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI THIELE, TODD ERIC · 2005 to 2014
$2.5M
CFR signaling in stress- and dependence- induced ethanol consumptionF31AA017803 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LOWERY-GIONTA, EMILY GEYER · 2008 to 2010
$90k
Ethanol-Induced Locomotor Sensitization: NPY Signaling and Chromatin RemodelingF31AA019839 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SPROW, GRETCHEN MARIE · 2010 to 2012
$86k
NIAAA NIH HHS AA013573NIAAA NIH HHS AA015148NIAAA NIH HHS AA017803NIAAA NIH HHS AA019839NIAAA NIH HHS F31 AA017803NIAAA NIH HHS F31 AA019839NIAAA NIH HHS R01 AA013573NIAAA NIH HHS R01 AA015148NIAAA NIH HHS R37 AA013573
6 · The paper itself

Abstract

Binge alcohol (ethanol) drinking is a destructive pattern of ethanol consumption that may precipitate ethanol dependence-a chronic, debilitating, and prevalent health problem. While an abundance of research has focused on the neurochemical underpinnings of ethanol dependence, relatively little is known about the mechanisms underlying the heavy consumption characteristic of binge ethanol drinking. Recently, a simple preclinical model termed "drinking in the dark" (DID) was developed to examine binge-like ethanol consumption in a rodent population. This assay capitalizes on the predisposition of C57BL/6J mice to voluntarily consume substantial quantities of a high concentration (20% v/v) ethanol solution, resulting in pharmacologically relevant blood ethanol concentrations (BECs). This review provides a comprehensive overview of recent literature utilizing this model to investigate the neuromodulatory systems that may influence binge ethanol drinking. Studies examining the glutamatergic and opioidergic systems not only provide evidence for these systems in the modulation of binge-like ethanol consumption, but also suggest this preclinical model has predictive validity and may be an appropriate tool for screening novel pharmacological compounds aimed at treating binge ethanol drinking in the human population. Additionally, this review presents evidence for the involvement of the GABAergic, dopaminergic, nicotinic, and endocannabinoid systems in modulating binge-like ethanol consumption. Finally, recent evidence shows that corticotropin-releasing factor (CRF), agouti-related protein (AgRP), neuropeptide Y (NPY), and ghrelin are also implicated as impacting this pattern of ethanol consumption.

Indexed as

NeurobiologyAgouti-Related ProteinAlcohol DrinkingAnimalsBinge-Eating DisorderCorticotropin-Releasing HormoneGhrelinHumansMiceMice, Inbred C57BLModels, AnimalAgouti-Related ProteinCorticotropin-Releasing HormoneGhrelin

Identifiers

PMID22245775
PMCPMC3348336
OpenAlexW2056359334

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.