Evidence map›Paper›PMID 28780411›Full record

ArticleBrain research bulletin2018

Increased ethanol drinking in "humanized" mice expressing the mu opioid receptor A118G polymorphism are mediated through sex-specific mechanisms.

Angela N Henderson-Redmond, Tammy E Lowe, Xi B Tian, Daniel J Morgan

Abstract read
In one paragraph

Article in Brain research bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Translational Research in Nicotine Addiction.Cold Spring Harbor perspectives in medicine · 2021
    Review
  4. Article
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 2 institutions in 1 country.

Angela N Henderson-RedmondDepartment of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States. Electronic address: ahenderson1@pennstatehealth.psu.edu.
Tammy E LoweDepartment of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States; Benedict College, Columbia, SC 29204, United States.
Xi B TianDepartment of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States.
Daniel J MorganDepartment of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States; Department of Pharmacology, Penn State University College of Medicine, Hershey, PA 17033, United States; Department of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey PA 17033, United States. Electronic address: dmorgan1@pennstatehealth.psu.edu.
Pennsylvania State University · USBenedict College · US

Funding

Characterization of a novel JNK-mediated mechanism of cannabinoid toleranceR21DA036385 · NIDA · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI MORGAN, DANIEL J · 2013 to 2014
$400k
NIDA NIH HHS R21 DA036385
6 · The paper itself

Abstract

The A118G single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (Oprm1) has been implicated in mediating the rewarding effects of alcohol. Clinical and preclinical studies suggest that the G allele may confer a genetic vulnerability to alcohol dependence, though it remains unknown whether these effects are sex-specific. We used male and female mice homozygous for the "humanized" 118AA or 118GG alleles to determine whether the A118G SNP potentiates ethanol consumption in a sex-specific manner in both the two-bottle choice and drinking-in-the-dark (DID) paradigms. Mice were also assessed for differences in naltrexone sensitivity, ethanol reward assessed via conditioned place preference (CPP), and sensitivity to the sedative/ataxic effects of ethanol using the rota-rod and loss of righting reflex (LORR) assays. We found that male and female 118GG mice drank significantly more ethanol than 118AA littermates using a continuous access, two-bottle choice paradigm. In the limited-access DID drinking model, (i) female (but not male) 118GG mice consumed more ethanol than 118AA mice and (ii) naltrexone pretreatment was equally efficacious at attenuating ethanol intake in both 118AA and 118GG female mice while having no effect in males. Male and female 118GG and female 118AA mice developed a robust conditioned place preference (CPP) for ethanol. Female 118GG mice displayed less sensitivity to the sedative/ataxic effects of ethanol compared to female 118AA mice on both the rota-rod and the LORR assays while male mice did not differ in their responses on either assay. Our findings suggest that increased ethanol consumption in male 118GG mice may be due to increased ethanol reward, while increased drinking in female 118GG mice might be due to decreased sensitivity to the sedative/ataxic effects of ethanol. Collectively, these data might be used to help identify sex-specific pharmacotherapies to combat alcohol use disorders.

Indexed as

Sex CharacteristicsAlcohol DrinkingAllelesAnalgesics, Non-NarcoticAnalysis of VarianceAnimalsChoice BehaviorConditioning, OperantDose-Response Relationship, DrugEthanolFemaleGenotypeMaleMiceMice, Inbred C57BLMice, TransgenicAnalgesics, Non-NarcoticEthanolnaltrexazoneNaltrexoneNarcotic AntagonistsOPRM1 protein, humanQuinineReceptors, Opioid, muA118GEthanolHumanized miceMu-opioid receptorSex differences

Identifiers

PMID28780411
PMCPMC5796878
OpenAlexW2741371760

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.