ArticleAlcohol (Fayetteville, N.Y.)2009
Differential activation of limbic circuitry associated with chronic ethanol withdrawal in DBA/2J and C57BL/6J mice.
Article in Alcohol (Fayetteville, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Septo-hypothalamic regulation of binge-like alcohol consumption by the nociceptin system.Cell reports · 2025Article
- Ethanol modulation of cortico-basolateral amygdala circuits: Neurophysiology and behavior.Neuropharmacology · 2021Review
- Dynamic c-Fos changes in mouse brain during acute and protracted withdrawal from chronic intermittent ethanol exposure and relapse drinking.Addiction biology · 2020Article
- From Pleasure to Pain, and Back Again: The Intricate Relationship Between Alcohol and Nociception.Alcohol and alcoholism (Oxford, Oxfordshire) · 2019Review
- Affective Disturbances During Withdrawal from Chronic Intermittent Ethanol Inhalation in C57BL/6J and DBA/2J Male Mice.Alcoholism, clinical and experimental research · 2018Article
- Ethanol withdrawal-induced dysregulation of neurosteroid levels in plasma, cortex, and hippocampus in genetic animal models of high and low withdrawal.Psychopharmacology · 2017Article
- Genetic studies of alcohol dependence in the context of the addiction cycle.Neuropharmacology · 2017Review
- Alignment of the transcriptome with individual variation in animals selectively bred for High Drinking-In-the-Dark (HDID).Alcohol (Fayetteville, N.Y.) · 2017Article
- Ethanol-Sensitive Pacemaker Neurons in the Mouse External Globus Pallidus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Limbic circuitry activation in ethanol withdrawal is regulated by a chromosome 1 locus.Alcohol (Fayetteville, N.Y.) · 2017Article
- Modulation of sensitivity to alcohol by cortical and thalamic brain regions.The European journal of neuroscience · 2016Article
- Article
- Chronic intermittent ethanol inhalation increases ethanol self-administration in both C57BL/6J and DBA/2J mice.Alcohol (Fayetteville, N.Y.) · 2015Article
- Acute ethanol withdrawal impairs contextual learning and enhances cued learning.Alcoholism, clinical and experimental research · 2015Article
- Understanding the addiction cycle: a complex biology with distinct contributions of genotype vs. sex at each stage.Neuroscience · 2014Article
- Chronic intermittent ethanol exposure and withdrawal alters (3α,5α)-3-hydroxy-pregnan-20-one immunostaining in cortical and limbic brain regions of C57BL/6J mice.Alcoholism, clinical and experimental research · 2014Article
- Ethosuximide reduces electrographical and behavioral correlates of alcohol withdrawal seizure in DBA/2J mice.Alcohol (Fayetteville, N.Y.) · 2014Article
- Local changes in neurosteroid levels in the substantia nigra reticulata and the ventral tegmental area alter chronic ethanol withdrawal severity in male withdrawal seizure-prone mice.Alcoholism, clinical and experimental research · 2013Article
- Effects of sodium butyrate on methamphetamine-sensitized locomotor activity.Behavioural brain research · 2013Article
- Modeling the diagnostic criteria for alcohol dependence with genetic animal models.Current topics in behavioral neurosciences · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Although no animal model exactly duplicates clinically defined alcoholism, models for specific factors, such as the withdrawal syndrome, are useful for identifying potential neural determinants of liability in humans. The well-documented difference in withdrawal severity following chronic ethanol exposure, between the DBA/2J and C57BL/6J mouse strains, provides an excellent starting point for dissecting the neural circuitry affecting predisposition to physical dependence on ethanol. To induce physical dependence, we used a paradigm in which mice were continuously exposed to ethanol vapor for 72h. Ethanol-exposed and air-exposed (control) mice received daily injections of pyrazole hydrochloride, an alcohol dehydrogenase inhibitor, to stabilize blood ethanol levels. Ethanol-dependent and air-exposed mice were killed 7h after removal from the inhalation chambers. This time point corresponds to the time of peak ethanol withdrawal severity. The brains were processed to assess neural activation associated with ethanol withdrawal indexed by c-Fos immunostaining. Ethanol-withdrawn DBA/2J mice showed significantly (P<.05) greater neural activation than ethanol-withdrawn C57BL/6J mice in the dentate gyrus, hippocampus CA3, lateral septum, basolateral and central nuclei of the amygdala, and prelimbic cortex. Taken together with results using an acute model, our data suggest that progression from acute ethanol withdrawal to the more severe withdrawal associated with physical dependence following chronic ethanol exposure involves recruitment of neurons in the hippocampal formation, amygdala, and prelimbic cortex. To our knowledge, these are the first studies to use c-Fos to identify the brain regions and neurocircuitry that distinguish between chronic and acute ethanol withdrawal severity using informative animal models.
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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.