ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Quantitative trait loci involved in genetic predisposition to acute alcohol withdrawal in mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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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.
The trial behind it
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Who cites it
77 citing papers in PubMed, 276 citations in OpenAlex.
- Aged female and male C57BL/6J mice have reduced alcohol self-administration and altered acute alcohol withdrawal compared to younger animals.Frontiers in aging neuroscience · 2026Article
- Identification of novel genetic loci and candidate genes for progressive ethanol consumption in diversity outbred mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Genome-wide association mapping of ethanol sensitivity in the Diversity Outbred mouse population.Alcoholism, clinical and experimental research · 2022Article
- Ethanol inhibition of lateral orbitofrontal cortex neuron excitability is mediated via dopamine D1/D5 receptor-induced release of astrocytic glycine.Neuropharmacology · 2021Article
- RNA-Seq Analysis of Genetic and Transcriptome Network Effects of Dual-Trait Selection for Ethanol Preference and Withdrawal Using SOT and NOT Genetic Models.Alcoholism, clinical and experimental research · 2020Article
- Article
- Genetic Contribution to Initial and Progressive Alcohol Intake Among Recombinant Inbred Strains of Mice.Frontiers in genetics · 2018Article
- Integrating Genetic and Gene Co-expression Analysis Identifies Gene Networks Involved in Alcohol and Stress Responses.Frontiers in molecular neuroscience · 2018Article
- Distinct Roles for Two Chromosome 1 Loci in Ethanol Withdrawal, Consumption, and Conditioned Place Preference.Frontiers in genetics · 2018Article
- Promising pharmacogenetic targets for treating alcohol use disorder: evidence from preclinical models.Pharmacogenomics · 2017Review
- Limbic circuitry activation in ethanol withdrawal is regulated by a chromosome 1 locus.Alcohol (Fayetteville, N.Y.) · 2017Article
- Analyses of differentially expressed genes after exposure to acute stress, acute ethanol, or a combination of both in mice.Alcohol (Fayetteville, N.Y.) · 2017Article
- A Spontaneous Mutation inFrontiers in pharmacology · 2017Article
- Effective Reduction of Acute Ethanol Withdrawal by the Tetracycline Derivative, Tigecycline, in Female and Male DBA/2J Mice.Alcoholism, clinical and experimental research · 2016Article
- Identification of quantitative trait loci and candidate genes for an anxiolytic-like response to ethanol in BXD recombinant inbred strains.Genes, brain, and behavior · 2016Article
- A Systems Approach Implicates a Brain Mitochondrial Oxidative Homeostasis Co-expression Network in Genetic Vulnerability to Alcohol Withdrawal.Frontiers in genetics · 2016Article
- Potentiation of Gamma Aminobutyric Acid Receptors (GABAAR) by Ethanol: How Are Inhibitory Receptors Affected?Frontiers in cellular neuroscience · 2016Review
- Transcriptome organization for chronic alcohol abuse in human brain.Molecular psychiatry · 2015Article
- Acute ethanol withdrawal impairs contextual learning and enhances cued learning.Alcoholism, clinical and experimental research · 2015Article
- Novel MPDZ/MUPP1 transgenic and knockdown models confirm Mpdz's role in ethanol withdrawal and support its role in voluntary ethanol consumption.Addiction biology · 2015Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Alcohol dependence (alcoholism) is accompanied by evidence of tolerance, withdrawal (physiological dependence), or compulsive behavior related to alcohol use. Studies of strain and individual differences using animal models for acute physiological dependence liability are useful means to identify potential genetic determinants of liability in humans. Behavioral and quantitative trait analyses were conducted using animal models for high risk versus resistance to acute physiological dependence. Using a two-step genetic mapping strategy, loci on mouse chromosomes 1, 4, and 11 were mapped that contain genes that influence alcohol withdrawal severity. In the aggregate, these three risk markers accounted for 68% of the genetic variability in alcohol withdrawal. Candidate genes in proximity to the chromosome 11 locus include genes encoding the alpha1, alpha6, and gamma2 subunits of type-A receptors for the inhibitory neurotransmitter, GABA. In addition, suggestive linkage is indicated for two loci on mouse chromosome 2, one near Gad1 encoding glutamic acid decarboxylase, and the other near the El2 locus which influences the seizure phenotype in the neurological mutant strain El. The present analyses detect and map some of the loci that increase risk to develop physiological dependence and may facilitate identification of genes related to the development of alcoholism. Syntenic conservation between human and mouse chromosomes suggests that human homologs of genes that increase risk for physiological dependence may localize to 1q21-q32, 2q24-q37/11p13, 9p21-p23/1p32-p22.1, and 5q32-q35.
Indexed as
Identifiers
9133412PMC6573712W1937687163What OpenQuestion holds
Registered trials
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.