Resilience to social stress coincides with functional DNA methylation of the Crf gene in adult mice
Abstract
DNA methylation regulates gene transcription and has been suggested to encode psychopathologies derived from early life stress. We found that methylation regulated the expression of the Crf (also known as Crh) gene and that chronic social stress in adult mice induced long-term demethylation of this genomic region. Demethylation was observed only in the subset of defeated mice that displayed social avoidance and site-specific knockdown of Crf attenuated the stress-induced social avoidance.
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Decreased levels of Dnmt3b were detected in CSDS mice.
“Researchers also detected decreased levels of Dnmt3b, but, more interestingly, it was observed that the viral knockdown of Crf in the PVN buffered against social avoidance behavior in CSDS mice.”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
Prolonged demethylation of the Crf promoter in adult mice that displayed social avoidance has been reported in a CSDS model, accompanied by a subsequent increase in Crf mRNA levels in the PVN of the hypothalamus.
“Prolonged demethylation of the Crf promoter in adult mice that displayed social avoidance has been reported in a CSDS model, accompanied by a subsequent increase in Crf mRNA levels in the PVN of the hypothalamus of these animals.”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
Increased Crf expression may underscore increased social anxiety behaviors in these animals by inducing HPA axis hyperactivity.
“This suggests that increased Crf expression may underscore increased social anxiety behaviors in these animals by inducing HPA axis hyperactivity (Elliott et al., 2010).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
Viral knockdown of Crf in the PVN buffered against social avoidance behavior in CSDS mice.
“it was observed that the viral knockdown of Crf in the PVN buffered against social avoidance behavior in CSDS mice.”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
Other candidate genes shown to be differentially methylated in rodent models include reelin (Reln), corticotropin-releasing hormone receptor (Crh), and arginine vasopressin gene (Avp).
“Other candidate genes shown to be differentially methylated include reelin (Reln) [39], which is involved in neurogenesis and synaptic plasticity, corticotropin-releasing hormone receptor (Crh) [40], which binds corticotropin-releasing hormone and plays an important role in stress signaling, and arginine vasopressin gene (Avp) [41].”
Early-life trauma in rodent models can influence DNA methylation of various candidate genes in brain regions important in stress signaling.
“Numerous subsequent studies using rodent models have shown that early-life trauma (e.g., chronic and unpredictable maternal behavior, separation, fear conditioning), can influence DNA methylation of various candidate genes in brain regions important in stress signaling.”
Both the Crf promoter demethylation and increased Crf mRNA findings were significantly reversed on administration of the antidepressant imipramine.
“Both findings were significantly reversed on administration of the antidepressant imipramine (Elliott et al., 2010).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
The CRH/Crf studies of Wang et al. (2013) and Elliott et al. (2010) show a direct correlation between Dnmt3b levels and CRF-associated genes in the PVN, suggesting that in this brain region Dnmt3b may be responsible for modulating their expression via methylation.
“The CRH/Crf studies of both Wang et al. (2013) and Elliott et al. (2010) show a direct correlation between Dnmt3b levels and CRF-associated genes in the PVN, suggesting that in this brain region, Dnmt3b may be responsible for modulating their expression via methylation.”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Elliott et al., 2010
An epigenetic mechanism induced by chronic stress in resilient mice only controls HPA axis hyperactivity.
“One recent paper found an epigenetic mechanism, induced by chronic stress in resilient mice only, that controls HPA axis hyperactivity83”
From Neurobiology of resilience (2012) · cites this paper as [83]
The Crh gene is hypermethylated and silenced to prevent Crh induction in resilient animals that lack social avoidance.
“the Crh gene is hypermethylated and silenced to prevent Crh induction in the subset of animals termed resilient for their lack of social avoidance”
From Neurobiology of resilience (2012) · cites this paper as [83]
After chronic social defeat stress, Crh gene expression is increased in the paraventricular nucleus of the hypothalamus of susceptible animals, and this adaptation is necessary for the development of social avoidance.
“after chronic social defeat stress, Crh gene expression is increased in the paraventricular nucleus (PVN) of hypothalamus of susceptible animals and that this adaptation is necessary for the development of social avoidance83”
From Neurobiology of resilience (2012) · cites this paper as [83]
Expression of a small interfering RNA to decrease CRH expression was sufficient to prevent social avoidance in susceptible mice.
“Expression of a small interfering RNA (RNAi) to decrease CRH expression was sufficient to prevent social avoidance in susceptible mice.”
From Neurobiology of resilience (2012) · cites this paper as [83]
DNA methylation appears to regulate hypothalamic corticotropin-releasing factor, an important modulator of the HPA axis.
“DNA methylation also appears to regulate hypothalamic corticotropin-releasing factor (CRF), an important modulator of the HPA axis.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [125]
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Solich, J., Kuśmider, M., Faron-Górecka, A., Pabian, P., & Dziedzicka-Wasylewska, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249469 · Cited by 13 · see citing works
- Authors
- Elliott, E., Ezra-Nevo, G., Regev, L., Neufeld-Cohen, A., & Chen, A.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Chen, Alon
- Venue
- Nature Neuroscience
- Published
- 2010-10-03
- Volume
- 13
- Issue
- 11
- Pages
- 1351-1353
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W1994388155
- Cited by
- 436
- References
- 16
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 12 · 2023: 13 · 2022: 21 · 2021: 26 · 2020: 27 · 2019: 21 · 2018: 26 · 2017: 41 · 2016: 43 · 2015: 39 · 2014: 49 · 2013: 38 · 2012: 26
- FWCI
- 13.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- corticotropin-releasing factor, DNA methylation, social stress, resilience, chronic social stress, demethylation, social avoidance, gene expression regulation, early life stress, psychopathology, knockout mice
- MeSH terms
- Decitabine, Cyclic AMP, Analysis of Variance, Animals, Antidepressive Agents, Tricyclic, Avoidance Learning, Azacitidine, Corticotropin-Releasing Hormone, Enzyme Inhibitors, Gene Expression Regulation, Genetic Vectors, Imipramine, Injections, Intraventricular, Male, Mice, Inbred C57BL, Naphthalenes, Neuroblastoma, Neurons, Oxepins, Paraventricular Hypothalamic Nucleus, RNA, Messenger, Stress, Psychological, DNA Methylation, RNA Interference, Microdissection, Cell Line, Tumor, Green Fluorescent Proteins, Mice
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