ArticleFrontiers in behavioral neuroscience2024
Chronic alcohol-induced long-lasting working memory deficits are associated with altered histone H3K9 dimethylation in the prefrontal cortex.
Article in Frontiers in behavioral neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Regulation of Chromatin Acetylation by Alcohol: Dependence on Sex, Brain Region, and Mode of Exposure.Genes · 2026Review
- Targeting G9a decreases escalated alcohol drinking in male mice in a model of combined stress and chronic alcohol exposure.Alcohol, clinical & experimental research · 2025Article
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6 authors at 2 institutions in 1 country.
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Abstract
Introduction: Epigenetic modifications have emerged as key contributors to the enduring behavioral, molecular and epigenetic neuroadaptations during withdrawal from chronic alcohol exposure. The present study investigated the long-term consequences of chronic alcohol exposure on spatial working memory (WM) and associated changes of transcriptionally repressive histone H3 lysine 9 dimethylation (H3K9me Methods: Male C57BL/6 mice were allowed free access to either 12% (v/v) ethanol for 5 months followed by a 3-week abstinence period or water. Spatial WM was assessed through the spontaneous alternation T-maze test. Alcoholic and water mice received daily injections of GABAB agonist baclofen or saline during alcohol fading and early withdrawal. Global levels of histone modifications were determined by immunohistochemistry. Results: Withdrawal mice displayed WM impairments along with reduced prefrontal H3K9me Conclusion: The findings suggest a role for long-lasting decreased H3K9me
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