Evidence map›Paper›PMID 31562845›Full record

ArticleNeuropharmacology2019

Pharmacological mechanisms of alcohol analgesic-like properties in mouse models of acute and chronic pain.

Bradley Neddenriep, Deniz Bagdas, Katherine M Contreras, Joseph W Ditre, Jennifer T Wolstenholme, Michael F Miles, M Imad Damaj

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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  13. The Dopamine System in Mediating Alcohol Effects in Humans.Current topics in behavioral neurosciences · 2025
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  15. Article
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  18. Alcohol use and the pain system.Advances in drug and alcohol research · 2024
    Review
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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

7 authors at 2 institutions in 1 country.

Bradley NeddenriepDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA.
Deniz BagdasDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA.
Katherine M ContrerasDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA.
Joseph W DitreDepartment of Psychology, Syracuse University, Syracuse, NY, USA.
Jennifer T WolstenholmeDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; VCU-Alcohol Research Center, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA.
Michael F MilesDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; VCU-Alcohol Research Center, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA.
M Imad DamajDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Virginia Commonwealth University, Richmond, VA, 23298-0613, USA. Electronic address: m.damaj@vcuhealth.org.
Virginia Commonwealth University · USSyracuse University · US

Funding

Project 5 - Genetic architecture of alcohol use disorder using cross-trait genetic correlations and public next-generation sequencing studiesP50AA022537 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI MICHAEL F MILES · 2014 to 2026
$19.6M
VCU Center for Drug Addiction ResearchP30DA033934 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI JOLENE J WINDLE · 2014 to 2026
$13.8M
Identification of gene variants for alcohol analgesiaR01AA027175 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI DAMAJ, M. IMAD, MILES, MICHAEL F · 2019 to 2023
$2.3M
Histone methylation as a potential mechanism for myelin deficits and behavioral alterations following adolescent binge ethanolR01AA026347 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI WOLSTENHOLME, JENNIFER T · 2018 to 2022
$1.7M
NIAAA NIH HHS P50 AA022537NIAAA NIH HHS R01 AA026347NIAAA NIH HHS R01 AA027175NIDA NIH HHS P30 DA033934
6 · The paper itself

Abstract

Alcohol use and chronic pain are highly comorbid. Acute alcohol use typically produces an analgesic effect. However, chronic use can worsen the progression of chronic pain. In rodent models, acute models of pain have primarily been used to investigate the relationship between alcohol and pain analgesia. Here, we use two models of chronic pain, chronic inflammatory and peripheral neuropathic pain, to investigate acute alcohol's antinociceptive and analgesic properties. We hypothesize that acute ethanol is acting through opioid receptors to create an analgesic-like effect in both reflexive and affective dimensions of pain. Using male and female C57BL/6J mice, oral ethanol administration (0-1.25 g/kg) showed a dose-dependent reversal of mechanical hypersensitivity in both Complete Freund's Adjuvant (CFA) and chronic constriction injury (CCI) models of chronic inflammatory and neuropathic pain. No sex differences were observed. Using the conditioned place preference (CPP) task to assess the subjective responses to ethanol's anti-nociceptive properties, CCI-injured animals showed a preference for the ethanol-paired side, suggesting a reduction in an aversive and pain-like state produced by nerve injury. These effects are likely mediated through the kappa and possibly the mu opioid systems, since ethanol-induced anti-nociception following CCI was fully reversed by pretreatment with the kappa selective antagonist, nor-BNI, or high doses of naltrexone. These data show that ethanol possesses analgesic-like properties in chronic inflammatory and neuropathic pain models in mice and provide new insight into ethanol as it relates to chronic pain.

Indexed as

Acute PainAdministration, OralAnalgesicsAnimalsChronic PainConditioning, PsychologicalDisease Models, AnimalEthanolFemaleInflammationMaleMiceMice, Inbred C57BLNeuralgiaSex CharacteristicsAnalgesicsEthanolAlcohol pain mice chronic

Identifiers

PMID31562845
PMCPMC6924270
OpenAlexW2977007813

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.