The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.
Epigenetic Mechanisms of Depression and Antidepressant Action
Open accessAbstract
Epigenetic mechanisms, which control chromatin structure and function, mediate changes in gene expression that occur in response to diverse stimuli. Recent research has established that environmental events and behavioral experience induce epigenetic changes at particular gene loci and that these changes help shape neuronal plasticity and function and hence behavior. Some of these changes can be stable and can even persist for a lifetime. Increasing evidence supports the hypothesis that aberrations in chromatin remodeling and subsequent effects on gene expression within limbic brain regions contribute to the pathogenesis of depression and other stress-related disorders such as post-traumatic stress disorder and other anxiety syndromes. Likewise, the gradually developing but persistent therapeutic effects of antidepressant medications may be achieved in part via epigenetic mechanisms. This review discusses recent advances in our understanding of the epigenetic regulation of stress-related disorders and focuses on three distinct aspects of stress-induced epigenetic pathology: the effects of stress and antidepressant treatment during adulthood, the lifelong effects of early-life stress on subsequent stress vulnerability, and the possible transgenerational transmission of stress-induced abnormalities.
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“In genetically susceptible models of treatment-resistant depression, SAHA inhibits HDAC2, restores histone acetylation and BDNF levels, and reverses antidepressant non-responsiveness (Meylan et al., 2016; Vialou et al., 2013).”
From Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook (2026) · cites this paper as Vialou et al., 2013
Experimental — accuracy not yet measuredIn the citing paper
“This maintains that depressed mood reflects an adaptive, risk-averse approach to social interaction that reduces the likelihood of further aversive outcomes by: (1) increasing our cognitive sensitivity to (sensory) cues of social risk; (2) reducing our (behavioural) propensity for taking social risks; and (3) initiating signalling behaviours that elicit support and defuse conflict [32].”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“This maintains that depressed mood reflects an adaptive, risk-averse approach to social interaction that reduces the likelihood of further aversive outcomes by: (1) increasing our cognitive sensitivity to (sensory) cues of social risk; (2) reducing our (behavioural) propensity for taking social risks; and (3) initiating signalling behaviours that elicit support and defuse conflict [32].”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“This maintains that depressed mood reflects an adaptive, risk-averse approach to social interaction that reduces the likelihood of further aversive outcomes by: (1) increasing our cognitive sensitivity to (sensory) cues of social risk; (2) reducing our (behavioural) propensity for taking social risks; and (3) initiating signalling behaviours that elicit support and defuse conflict [32].”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“This maintains that depressed mood reflects an adaptive, risk-averse approach to social interaction that reduces the likelihood of further aversive outcomes by: (1) increasing our cognitive sensitivity to (sensory) cues of social risk; (2) reducing our (behavioural) propensity for taking social risks; and (3) initiating signalling behaviours that elicit support and defuse conflict [32].”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“The depressive response is adaptive when changes in mood state and behaviour reduce uncertainty in the face of socio-environmental change, and lead to re-engagement with that environment when volatility abates (which should, at least in part, be brought about by depressive behaviours; see [32]).”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“Notably, the exacerbation of normative depressed states into severe, dysfunctional forms is also likely when depressive changes fail to alleviate social stress, creating a self-perpetuating cycle arising from heightened and prolonged arousal of ineffectual attempts to reduce socio-environmental volatility [32].”
From The depressed brain: an evolutionary systems theory (2017) · cites this paper as [32]
In the citing paper
“Cholinergic innervation has been known for a long time to regulate critical period plasticity209.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [209]
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Items 201–216 of 216
Gould, T. D., O’Donnell, K. C., Picchini, A. M., Dow, E. R., Chen, G., & Manji, H. K. (2008) · Behavioural Brain Research · doi:10.1016/j.bbr.2007.12.028 · Cited by 74
Chertkow-Deutsher, Y., Cohen, H., Klein, E., & Ben‐Shachar, D. (2009) · The International Journal of Neuropsychopharmacology · doi:10.1017/s146114570999071x · Cited by 73
Minireview: NAD+, a Circadian Metabolite with an Epigenetic Twist
Sassone-Corsi, P. (2012) · Endocrinology · doi:10.1210/en.2011-1535 · Cited by 71
The methyl-CpG-binding protein MeCP2 and neurological disease
Bird, A. P. (2008) · Biochemical Society Transactions · doi:10.1042/bst0360575 · Cited by 69
What Are Imprinted Genes Doing in the Brain?
Davies, W., Isles, A. R., Humby, T., & Wilkinson, L. S. (2008) · Advances in experimental medicine and biology · doi:10.1007/978-0-387-77576-0_5 · Cited by 68
Conway-Campbell, B. L., George, C. L., Pooley, J. R., Knight, D. M., Norman, M. R., Hager, G. L., & Lightman, S. L. (2011) · Molecular Endocrinology · doi:10.1210/me.2010-0073 · Cited by 67
Hinwood, M., Tynan, R. J., Day, T. A., & Walker, F. R. (2010) · Cerebral Cortex · doi:10.1093/cercor/bhq080 · Cited by 58
CpG Methylation in Neurons: Message, Memory, or Mask?
Sharma, R. P., Gavin, D. P., & Grayson, D. R. (2010) · Neuropsychopharmacology · doi:10.1038/npp.2010.85 · Cited by 43
The road not taken: life experiences in monozygotic twin pairs discordant for major depression
Kendler, K. S., & Halberstadt, L. J. (2012) · Molecular Psychiatry · doi:10.1038/mp.2012.55 · Cited by 41
Cuzin, F., & Rassoulzadegan, M. (2010) · Essays in Biochemistry · doi:10.1042/bse0480101 · Cited by 38
Nestler, E. J. (2011) · Scientific American · doi:10.1038/scientificamerican1211-76 · Cited by 36
Self-citationIntrauterine factors as determinants of depressive disorder.
Weinstock, M. (2010) · PubMed · Cited by 33
What Are Imprinted Genes Doing in the Brain?
Davies, W., Isles, A. R., Humby, T., & Wilkinson, L. S. (2007) · Epigenetics · doi:10.4161/epi.2.4.5379 · Cited by 25
Le-Niculescu, H., Patel, S. D., & Niculescu, A. B. (2010) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2010.08.008 · Cited by 13
Rassoulzadegan, M., & Cuzin, F. (2010) · Organogenesis · doi:10.4161/org.6.1.11094 · Cited by 10
Chromatin-Based Treatments for Affective Disorders – Insight or Utopia
Covington, H. E., & Berton, O. (2010) · Modern trends in psychiatry · doi:10.1159/000319526 · Cited by 1
Research works printed but not linked: 2
- Anisman H, 2008, J. Psychiatry Neurosci., 33, 131
- Weinstock M, 2010, Isr. J. Psychiatry Relat. Sci., 47, 36
Cited by
Sorted by citations
Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206
Management of Depression in Older Adults: A Review
Kok, R. M., & Reynolds, C. F. (2017) · JAMA · doi:10.1001/jama.2017.5706 · Cited by 890
Sex-specific transcriptional signatures in human depression
Labonté, B., Engmann, O., Purushothaman, I., Menard, C., Wang, J., Tan, C., Scarpa, J. R., Moy, G., Loh, Y.-H. E., Cahill, M., et al. (2017) · Nature Medicine · doi:10.1038/nm.4386 · Cited by 748
Self-citationThe organization of the stress system and its dysregulation in depressive illness
Gold, P. W. (2015) · Molecular Psychiatry · doi:10.1038/mp.2014.163 · Cited by 654
Epigenetics of the depressed brain: role of histone acetylation and methylation
Sun, H., Kennedy, P. J., & Nestler, E. J. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2012.73 · Cited by 413
Self-citation
Metadata
- Authors
- Vialou, V., Feng, J., Robison, A. J., & Nestler, E. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Nestler, Eric J.
- Venue
- Annual Review of Pharmacology and Toxicology
- Publisher
- Annual Reviews
- Published
- 2013-01-06
- Volume
- 53
- Issue
- 1
- Pages
- 59-87
- ISSN
- 0362-1642 (ISSN-L)
- 1545-4304
- PMC
- PMC3711377
- OpenAlex
- W2130374405
- Cited by
- 277
- References
- 216
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 12 · 2023: 11 · 2022: 13 · 2021: 18 · 2020: 14 · 2019: 26 · 2018: 26 · 2017: 25 · 2016: 32 · 2015: 32 · 2014: 26 · 2013: 21
- FWCI
- 1.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Annual Review of Pharmacology and Toxicology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (P50MH096890, R01MH051399)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- epigenetics, depression, antidepressant mechanism, chromatin remodeling, neuroplasticity, limbic system, post-traumatic stress disorder, anxiety, early life stress, stress vulnerability, transgenerational transmission, gene expression regulation
- MeSH terms
- Animals, Antidepressive Agents, Depression, Humans, Gene Expression, DNA Methylation, Epigenesis, Genetic
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