Antidepressant Actions of Histone Deacetylase Inhibitors
Open accessAbstract
Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin remodeling. We find that chronic social defeat stress in mice causes a transient decrease, followed by a persistent increase, in levels of acetylated histone H3 in the nucleus accumbens, an important limbic brain region. This persistent increase in H3 acetylation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens. Similar effects were observed in the nucleus accumbens of depressed humans studied postmortem. These changes in H3 acetylation and HDAC2 expression mediate long-lasting positive neuronal adaptations, since infusion of HDAC inhibitors into the nucleus accumbens, which increases histone acetylation, exerts robust antidepressant-like effects in the social defeat paradigm and other behavioral assays. HDAC inhibitor [ N -(2-aminophenyl)-4-[ N -(pyridine-3-ylmethoxy-carbonyl)aminomethyl]benzamide (MS-275)] infusion also reverses the effects of chronic defeat stress on global patterns of gene expression in the nucleus accumbens, as determined by microarray analysis, with striking similarities to the effects of the standard antidepressant fluoxetine. Stress-regulated genes whose expression is normalized selectively by MS-275 may provide promising targets for the future development of novel antidepressant treatments. Together, these findings provide new insight into the underlying molecular mechanisms of depression and antidepressant action, and support the antidepressant potential of HDAC inhibitors and perhaps other agents that act at the level of chromatin structure.
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Case/control differences in histone acetylation and methylation have been observed in depression.
“Like with DNAm, case/control differences in depression have been observed.”
From Epigenetics and depression (2019) · cites this paper as [19]
The Results section reports significantly higher histone H3 acetylation in postmortem nucleus accumbens tissue from depressed individuals than from matched controls. It does not report a depression case/control difference in histone methylation; the copy’s reference to demethylation concerns a cited study of antidepressant medications. (LLM, conf=0.88)
Experimental — accuracy not yet measuredHDAC inhibitors such as valproic acid and sodium butyrate can restore normal gene expression in psychiatric conditions.
“HDAC inhibitors such as valproic acid and sodium butyrate can restore normal gene expression in psychiatric conditions”
From The clinical use of epigenetics in psychiatry: a narrative review of epigenetic mechanisms, key candidate genes, and precision psychiatry (2025) · cites this paper as [28]
The Results section reports that the HDAC inhibitor MS-275 generally reversed stress-induced gene-expression changes in the nucleus accumbens of mice. It does not show that valproic acid or sodium butyrate restored gene expression, and the finding is limited to a mouse model of depression rather than psychiatric conditions generally; page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMolecular studies have identified similarities in chromatin remodeling and transcriptional activation between resilient and antidepressant-treated mice, providing new information about therapeutic targets.
“In addition, molecular studies have identified similarities in chromatin remodeling29,30 and transcriptional activation31 between resilient and antidepressant-treated mice, providing new information about therapeutic targets.”
From A standardized protocol for repeated social defeat stress in mice (2011) · cites this paper as [29]
The Abstract and Discussion describe chromatin changes after social defeat and antidepressant-like effects of HDAC inhibition, supporting a link between chromatin remodeling and potential treatments. But the paper does not compare resilient mice with antidepressant-treated mice; the Discussion says fluoxetine did not produce the H3 acetylation or HDAC2 changes associated with HDAC inhibition. Its reported similarity is in gene-expression effects of two treatments, not between resilient and treated mice (Results, page unavailable). (LLM, conf=0.83)
Experimental — accuracy not yet measuredHDAC2 was downregulated in the nucleus accumbens of patients with MDD compared with controls.
“Accordingly, a downregulation of HDAC2 was observed in these patients.”
From Epigenetics and depression (2019) · cites this paper as [19]
Global acetylation of H3K14ac was increased in the nucleus accumbens in postmortem tissue of patients with MDD compared with psychiatrically healthy controls.
“Global acetylation of the histone 3 at lysine 14 (H3K14ac), a modification shown to be dynamically regulated by social defeat in rodent models in various brain regions, 17 , 18 was increased in the nucleus accumbens (NAc) taken from postmortem tissue of patients with MDD vs psychiatrically healthy controls.”
From Epigenetics and depression (2019) · cites this paper as [19]
Infusion of the HDAC inhibitor MS-275 into the NAc reversed global gene expression patterns in the NAc and improved depression-like behaviors.
“Infusion of HDAC inhibitors (i.e., MS-275) into the NAc reversed global gene expression patterns in the NAc and improved depression-like behaviors.”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [130]
Mice exposed to chronic social defeat stress experienced a temporary reduction followed by a lasting escalation in H3K14 acetylation, connected to decreased HDAC2 levels in the NAc.
“mice exposed to chronic social defeat stress experienced a temporary reduction followed by a lasting escalation in histone acetylation levels (H3K14ac), which was connected to decreased histone deacetylase 2 (HDAC2) levels in the NAc.130”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [130]
Differential brain expression of HDACs was found in postmortem tissue in MDD.
“differential brain expression of HDACs was found in the postmortem in MDD.130,159”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [130]
HDAC inhibitors can increase DRD2 expression in certain contexts.
“Histone deacetylase inhibitors (HDACi) can increase DRD2 expression in certain contexts”
From The clinical use of epigenetics in psychiatry: a narrative review of epigenetic mechanisms, key candidate genes, and precision psychiatry (2025) · cites this paper as [28]
The Results section reports that HDAC inhibitor MS-275 changes gene expression in the nucleus accumbens, but it does not identify DRD2 among the affected genes. Searches for “DRD2 expression” and “dopamine receptor D2” found no passage in our copy stating that an HDAC inhibitor increases its expression. (LLM, conf=0.73)
Experimental — accuracy not yet measuredAnhedonic and metabolic symptoms in susceptible mice are maladaptive and are reversed by chronic antidepressant administration.
“The anhedonic and metabolic symptoms are clearly maladaptive and indeed are reversed by chronic administration of antidepressants to susceptible mice36, 37.”
From Neurobiology of resilience (2012) · cites this paper as [37]
In rodents, chronic stress affects the total levels of acetylated histones in certain limbic regions.
“In rodents, chronic stress affects the total levels of acetylated histones in certain limbic regions.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [66]
Suberoylanilide hydroxamic acid has a rapid antidepressant action and may be effective for depressive-like behaviors in mice that are resistant to conventional treatments.
“other reports have also shown that SAHA has a rapid antidepressant action 66 and that SAHA treatment may be effective for depressive-like behaviors in mice that are resistant to conventional treatments.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [66]
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- Authors
- Covington, H. E., Maze, I., LaPlant, Q. C., Vialou, V. F., Ohnishi, Y. N., Berton, O., Fass, D. M., Renthal, W., Rush, A. J., Wu, E. Y., Ghose, S., Krishnan, V., Russo, S. J., Tamminga, C., Haggarty, S. J., & Nestler, E. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- University of Pennsylvania (US)
- The University of Texas Southwestern Medical Center (US)
- Broad Institute (US)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2009-09-16
- Volume
- 29
- Issue
- 37
- Pages
- 11451-11460
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2775805
- OpenAlex
- W2028679671
- Cited by
- 624
- References
- 63
- Citations by year
- 2026: 13 · 2025: 22 · 2024: 28 · 2023: 16 · 2022: 33 · 2021: 33 · 2020: 29 · 2019: 35 · 2018: 43 · 2017: 41 · 2016: 54 · 2015: 33 · 2014: 48 · 2013: 46 · 2012: 56
- FWCI
- 20.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- Funders
- AstraZeneca
- National Institute of Mental Health (R01MH051399, P50MH066172)
- National Institute on Drug Abuse (R01DA028301)
- 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
- histone deacetylase inhibitors, antidepressant mechanism, depression, chronic social defeat stress, histone H3 acetylation, HDAC2, nucleus accumbens, chromatin remodeling, entinostat, gene expression regulation, fluoxetine, postmortem brain
- MeSH terms
- Vorinostat, Analysis of Variance, Animals, Antidepressive Agents, Behavior, Animal, Benzamides, Depression, Disease Models, Animal, Dominance-Subordination, Dose-Response Relationship, Drug, Enzyme Inhibitors, Fluoxetine, Food Preferences, Histone Deacetylases, Histones, Humans, Hydroxamic Acids, Interpersonal Relations, Male, Mice, Inbred C57BL, Models, Biological, Nucleus Accumbens, Postmortem Changes, Pyridines, Repressor Proteins, RNA, Messenger, Sucrose, Sweetening Agents, Gene Expression Regulation, Enzymologic, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Mice, Histone Deacetylase 2, Histone Deacetylase Inhibitors
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