ArticleNeurobiology of stress2021
Stress-induced visceral pain in female rats is associated with epigenetic remodeling in the central nucleus of the amygdala.
Article in Neurobiology of stress, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Duloxetine as a gut-brain axis modulator in irritable bowel syndrome: neuroimmune, microbiota, and pharmacogenomic perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Central control of gastrointestinal functions in health and disease.Physiological reviews · 2026Review
- Article
- The relation between clinical characteristics and mental health in patients with rheumatoid arthritis.Scientific reports · 2025Article
- Upregulation of KDM6B in the anterior cingulate cortex contributes to neonatal maternal deprivation-induced chronic visceral pain in mice.Molecular pain · 2024Article
- Research Progress of Central and Peripheral Corticotropin-Releasing Hormone in Irritable Bowel Syndrome with Comorbid Dysthymic Disorders.Gut and liver · 2024Review
- Review
- Modulation of visceral pain by brain nuclei and brain circuits and the role of acupuncture: a narrative review.Frontiers in neuroscience · 2023Review
- Epigenetic modulation of visceral nociception.Neurogastroenterology and motility · 2022Review
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Stress and anxiety contribute to the pathophysiology of irritable bowel syndrome (IBS), a female-predominant disorder of the gut-brain axis, characterized by abdominal pain due to heightened visceral sensitivity. In the current study, we aimed to evaluate in female rats whether epigenetic remodeling in the limbic brain, specifically in the central nucleus of the amygdala (CeA), is a contributing factor in stress-induced visceral hypersensitivity. Our results showed that 1 h exposure to water avoidance stress (WAS) for 7 consecutive days decreased histone acetylation at the GR promoter and increased histone acetylation at the CRH promoter in the CeA. Changes in histone acetylation were mediated by the histone deacetylase (HDAC) SIRT-6 and the histone acetyltransferase CBP, respectively. Administration of the HDAC inhibitor trichostatin A (TSA) into the CeA prevented stress-induced visceral hypersensitivity through blockade of SIRT-6 mediated histone acetylation at the GR promoter. In addition, HDAC inhibition within the CeA prevented stress-induced histone acetylation of the CRH promoter. Our results suggest that, in females, epigenetic modifications in the limbic brain regulating GR and CRH expression contribute to stress-induced visceral hypersensitivity and offer a potential explanation of how stress can trigger symptoms in IBS patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.