ArticleNeuropharmacology2020
Chronic alcohol exposure reduces acetylated histones in the sleep-wake regulatory brain regions to cause insomnia during withdrawal.
Article in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Epigenetic Insights and Exosome-Based Therapeutics for Insomnia: Bridging Sleep Biology and Precision Medicine.Molecular neurobiology · 2026Review
- Regulation of Chromatin Acetylation by Alcohol: Dependence on Sex, Brain Region, and Mode of Exposure.Genes · 2026Review
- Protein Acylation Modifications in Sleep Disorders: Mechanisms and Therapeutic Potential.Journal of molecular neuroscience : MN · 2026Review
- A ventral pallidum-locus coeruleus-lateral hypothalamus pathway modulates brain arousal in freely behaving and isoflurane-anesthetized male mice.Nature communications · 2025Article
- Alcohol induces long-lasting sleep deficits in Drosophila via subsets of cholinergic neurons.Current biology : CB · 2025Article
- Impact of Developmental Alcohol Exposure on Sleep Physiology.Advances in experimental medicine and biology · 2025Review
- Chronic alcohol-induced long-lasting working memory deficits are associated with altered histone H3K9 dimethylation in the prefrontal cortex.Frontiers in behavioral neuroscience · 2024Article
- The Impact of Alcohol-Induced Epigenetic Modifications in the Treatment of Alcohol use Disorders.Current medicinal chemistry · 2024Review
- Emerging Single-Cell Technological Approaches to Investigate Chromatin Dynamics and Centromere Regulation in Human Health and Disease.International journal of molecular sciences · 2021Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlcohol use disorder (AUD) develops after chronic and heavy use of alcohol. Insomnia, a hallmark of AUD, plays a crucial role in the development of AUD. However, the causal mechanisms are unknown. Since chronic alcohol reduces acetylated histones and disrupts the epigenome, we hypothesized that chronic alcohol exposure will reduce acetylated histones in wake-promoting regions of the brain to cause insomnia during alcohol withdrawal.
methodsAdult male C57BL/6J mice, surgically instrumented for electrophysiological monitoring of sleep-wakefulness, were exposed to chronic alcohol (6.8%) consumption using Lieber-DeCarli liquid diet. Three experiments were performed. First, the effect of chronic alcohol consumption was examined on sleep-wakefulness during 7 days of withdrawal. Second, the expression of acetylated histones, H3 lysine 14 (AcH3K14), was examined in two major sleep-wake regulatory brain regions: basal forebrain (BF) and lateral hypothalamus (LH) of the brain by using western blotting. Next, blockade of histone deacetylase, via systemic administration of TSA was examined on alcohol-induced changes in sleep-wakefulness.
resultsAlcoholic mice displayed a significant reduction in the quality and quantity of NREM sleep coupled with a significant increase in wakefulness that lasted for several days during alcohol withdrawal. In addition, alcoholic mice displayed a significant reduction in the expression of AcH3K14 in both BF and LH. Systemic administration of TSA significantly attenuated insomnia and improved the quality and quantity of sleep during alcohol withdrawal.
conclusionsBased on our results, we suggest that a causal relationship exists between reduced histone acetylation and insomnia during alcohol withdrawal.
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