The histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) alleviates depression-like behavior and normalizes epigenetic changes in the hippocampus during ethanol withdrawal
Open accessAbstract
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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In cognitive impairment models, SAHA increases histone acetylation, enhances BDNF expression, and strengthens antioxidant defenses, thereby improving learning and memory.
“In cognitive impairment models, it increases histone acetylation, enhances BDNF expression, and strengthens antioxidant defenses, thereby improving learning and memory (Chen et al., 2019; Amiri et al., 2017; Sadeghi et al., 2016).”
From Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook (2026) · cites this paper as Chen et al., 2019
The Results section (page unavailable) reports that SAHA restored reduced histone H3K9 acetylation to control levels in the hippocampal CA3 region of rats during ethanol withdrawal. The Discussion treats BDNF as a possible downstream target, not a measured SAHA effect. This paper does not establish stronger antioxidant defenses or improved learning and memory in cognitive-impairment models. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe broad-spectrum HDAC inhibitor SAHA exhibits antidepressant effects across multiple animal models, with benefits that extend beyond mood improvement.
“The broad-spectrum HDAC inhibitor SAHA exhibits antidepressant effects across multiple animal models, with benefits that extend beyond mood improvement (Nasehi et al., 2022; Ershadi et al., 2021; Chen et al., 2019; Meylan et al., 2016).”
From Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook (2026) · cites this paper as Chen et al., 2019
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- Authors
- Chen, W.-Y., Zhang, H., Gatta, E., Glover, E. J., Pandey, S. C., & Lasek, A. W.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Lasek, Amy W.
- Venue
- Alcohol
- Publisher
- Elsevier BV
- Published
- 2019-08
- Volume
- 78
- Pages
- 79-87
- ISSN
- 0741-8329 (ISSN-L)
- PMC
- PMC6612300
- OpenAlex
- W2920921721
- Cited by
- 59
- References
- 69
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 11 · 2023: 5 · 2022: 8 · 2021: 12 · 2020: 12 · 2019: 1
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Alcohol (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- vorinostat, histone deacetylase inhibitors, HDAC2, histone acetylation, H3K9 acetylation, ethanol withdrawal, alcoholism, hippocampus, epigenetic regulation, depression-like behavior, chronic ethanol exposure
- MeSH terms
- Vorinostat, Acetylation, Animals, Depression, Hippocampus, Histones, Male, Substance Withdrawal Syndrome, Rats, Sprague-Dawley, Epigenesis, Genetic, Rats, Histone Deacetylase 2, Histone Deacetylase Inhibitors
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