ArticleAlcohol (Fayetteville, N.Y.)2019
The histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal.
Article in Alcohol (Fayetteville, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Regulation of Chromatin Acetylation by Alcohol: Dependence on Sex, Brain Region, and Mode of Exposure.Genes · 2026Review
- Early life adversity, oxytocin system alterations, and addiction vulnerability: a narrative review.Psychopharmacology · 2026Review
- Epigenetic Basis of Stress-Induced Central Nervous System Disorders: Therapeutic Approaches.Biology · 2026Review
- Addictive drug abuse and depression-a focus on epigenetics.Communications biology · 2026Review
- Modifications on histone tails in psychiatric disorders.EC psychology and psychiatry · 2026Article
- Molecular insights into trauma: A framework of epigenetic pathways to resilience through intervention.Med (New York, N.Y.) · 2025Review
- Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook.Frontiers in genetics · 2025Review
- Identification of gene signatures and potential pharmaceutical candidates linked to COVID-19-related depression based on gene expression profiles.Frontiers in pharmacology · 2025Article
- The Promise of Epigenetic Editing for Treating Brain Disorders.Sub-cellular biochemistry · 2025Review
- Epigenetic drugs and psychedelics as emerging therapies for alcohol use disorder: insights from preclinical studies.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Review
- Histone deacetylase inhibitor decreases hyperalgesia in a mouse model of alcohol withdrawal-induced hyperalgesia.Alcohol, clinical & experimental research · 2024Article
- Transcriptional Dysregulation of Cholesterol Synthesis Underlies Hyposensitivity to GABA in the Ventral Tegmental Area During Acute Alcohol Withdrawal.Biological psychiatry · 2024Article
- Effects of entinostat, quisinostat, and tubastatin-A on alcohol consumption in male high ethanol consuming rats.Frontiers in epigenetics and epigenomics · 2024Article
- Trichostatin A relieves anxiety-and depression-like symptoms in APP/PS1 mice.Frontiers in pharmacology · 2024Article
- Chronic alcohol-induced long-lasting working memory deficits are associated with altered histone H3K9 dimethylation in the prefrontal cortex.Frontiers in behavioral neuroscience · 2024Article
- Conserved role for PCBP1 in altered RNA splicing in the hippocampus after chronic alcohol exposure.Molecular psychiatry · 2023Article
- Suberoylanilide Hydroxamic Acid (SAHA) Is a Driver Molecule of Neuroplasticity: Implication for Neurological Diseases.Biomolecules · 2023Review
- Molecular Toxicology and Pathophysiology of Comorbid Alcohol Use Disorder and Post-Traumatic Stress Disorder Associated with Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- Chronic ethanol consumption exacerbates future stress-enhanced fear learning, an effect mediated by dorsal hippocampal astrocytes.Alcoholism, clinical and experimental research · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Withdrawal from chronic alcohol drinking can cause depression, leading to an inability to function in daily life and an increased risk for relapse to harmful drinking. Understanding the causes of alcohol withdrawal-related depression may lead to new therapeutic targets for treatment. Epigenetic factors have recently emerged as important contributors to both depression and alcohol use disorder (AUD). Specifically, acetylation of the N-terminal tails of histone proteins that package DNA into nucleosomes is altered in stress-induced models of depression and during alcohol withdrawal. The goal of this study was to examine depression-like behavior during alcohol withdrawal and associated changes in histone acetylation and expression of histone deacetylase 2 (HDAC2) in the hippocampus, a brain region critical for mood regulation and depression. Male Sprague-Dawley rats were treated with the Lieber-DeCarli ethanol liquid diet for 15 days and then underwent withdrawal. Rats were treated with the HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA), during withdrawal and were tested for depression-like behavior. In a separate group of rats, the hippocampus was analyzed for mRNA and protein expression of HDAC2 and levels of histone H3 lysine 9 acetylation (H3K9ac) during chronic ethanol exposure and withdrawal. Rats undergoing ethanol withdrawal exhibited depression-like behavior and had increased HDAC2 and decreased H3K9ac levels in specific structures of the hippocampus. Treatment with SAHA during withdrawal ameliorated depression-like behavior and normalized changes in hippocampal HDAC2 and H3K9ac levels. These results demonstrate that ethanol withdrawal causes an altered epigenetic state in the hippocampus. Treatment with an HDAC inhibitor can correct this state and alleviate depression-like symptoms developed during withdrawal. Targeting histone acetylation may be a novel strategy to reduce ethanol withdrawal-induced depression.
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