ArticleAlcohol, clinical & experimental research2024
Histone deacetylase inhibitor decreases hyperalgesia in a mouse model of alcohol withdrawal-induced hyperalgesia.
Article in Alcohol, clinical & experimental research, 2024. 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, 9 citations in OpenAlex.
- The analgesic effect of neuropeptide S (NPS) in alcohol-dependent male and female rats.Alcohol (Fayetteville, N.Y.) · 2026Article
- Alcohol use disorder-associated pain: clinical and preclinical evidence.Alcohol (Fayetteville, N.Y.) · 2025Review
- A conceptual framework for the intersection of hyperalgesia and hyperkatifeia in alcohol addiction.Alcohol (Fayetteville, N.Y.) · 2025Review
- Chronic alcohol drinking delays recovery from capsaicin- and nerve injury-induced hypersensitivity in mice.Alcohol (Fayetteville, N.Y.) · 2025Article
- Targeting IL-6 as a novel therapeutic approach for alcohol abstinence - related mechanical allodynia.Neuropharmacology · 2025Article
- Alcohol addiction and Alzheimer's disease: a molecular collision course.Translational psychiatry · 2025Review
- Chronic alcohol drinking delays recovery from capsaicin- and nerve injury-induced hypersensitivity in mice.bioRxiv : the preprint server for biology · 2025Article
- Analgesic effect of oxytocin in alcohol-dependent male and female rats.Alcohol (Fayetteville, N.Y.) · 2025Article
- Modulation of stress-, pain-, and alcohol-related behaviors by perineuronal nets.Neurobiology of stress · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlcohol withdrawal-induced hyperalgesia (AWH) is characterized as an increased pain sensitivity observed after cessation of chronic alcohol use. Alcohol withdrawal-induced hyperalgesia can contribute to the negative affective state associated with abstinence and can increase susceptibility to relapse. We aimed to characterize pain sensitivity in mice during withdrawal from two different models of alcohol exposure: chronic drinking in the dark (DID) and the Lieber-DeCarli liquid diet. We also investigated whether treatment with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), could ameliorate AWH in mice treated with the Lieber-DeCarli diet.
methodsMale and female C57BL/6J mice were used for these studies. In the DID model, mice received bottles of 20% ethanol or water during the dark cycle for 4 h per day on four consecutive days per week for 6 weeks. Peripheral mechanical sensitivity was measured weekly the morning of Day 5 using von Frey filaments. In the Lieber-DeCarli model, mice received ethanol (5% v/v) or control liquid diet for 10 days, along with a single binge ethanol gavage (5 g/kg) or control gavage, respectively, on Day 10. Peripheral mechanical sensitivity was measured during the liquid diet administration and at 24 and 72 h into ethanol withdrawal. An independent group of mice that received the Lieber-DeCarli diet were administered SAHA (50 mg/kg, i.p.) during withdrawal.
resultsMale mice exhibited mechanical hypersensitivity after consuming ethanol for 5 weeks in the DID procedure. In the Lieber-DeCarli model, ethanol withdrawal led to hyperalgesia in both sexes. Suberoylanilide hydroxamic acid treatment during withdrawal from the ethanol liquid diet alleviated AWH.
conclusionsThese results demonstrate AWH in mice after chronic binge drinking in males and after Lieber-DeCarli liquid diet administration in both sexes. Like previous findings in rats, HDAC inhibition reduced AWH in mice, suggesting that epigenetic mechanisms are involved in AWH.
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