ArticleMolecular pain2016
Estrogen-dependent visceral hypersensitivity following stress in rats: An fMRI study.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Central control of gastrointestinal functions in health and disease.Physiological reviews · 2026Review
- Preclinical perspectives on disorders of the temporomandibular joint: Tracing the past, navigating the present, and shaping the future.The journal of pain · 2025Review
- Neural circuit basis of placebo pain relief.Nature · 2024Article
- Paraventricular Mast Cell-Derived Histamine Activates CRH Neurons to Mediate Adult Visceral Hypersensitivity Induced by Neonatal Maternal Separation.Brain sciences · 2023Article
- Electroacupuncture in the treatment of IBS in rats: investigation of the mechanisms of CRHJournal of neurophysiology · 2023Article
- Regional brain activation during rectal distention and attenuation with alosetron in a nonhuman primate model of irritable bowel syndrome.FASEB bioAdvances · 2022Article
- [Hippocampus is involved in 17β-estradiol exacerbating experimental occlusal inter- ference-induced chronic masseter hyperalgesia in ovariectomized rats].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022Article
- Gut feelings: the microbiota-gut-brain axis on steroids.American journal of physiology. Gastrointestinal and liver physiology · 2022Review
- Stress-induced visceral pain in female rats is associated with epigenetic remodeling in the central nucleus of the amygdala.Neurobiology of stress · 2021Article
- Differential Activation of Colonic Afferents and Dorsal Horn Neurons Underlie Stress-Induced and Comorbid Visceral Hypersensitivity in Female Rats.The journal of pain · 2021Article
- Estrogen receptors in pain modulation: cellular signaling.Biology of sex differences · 2021Review
- Sex-Bias in Irritable Bowel Syndrome: Linking Steroids to the Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- Left and right hemispheric lateralization of the amygdala in pain.Progress in neurobiology · 2021Review
- Peripheral mechanisms contribute to comorbid visceral hypersensitivity induced by preexisting orofacial pain and stress in female rats.Neurogastroenterology and motility · 2020Article
- Animal Models for Functional Gastrointestinal Disorders.Frontiers in psychiatry · 2020Review
- Importance of Non-pharmacological Approaches for Treating Irritable Bowel Syndrome: Mechanisms and Clinical Relevance.Frontiers in pain research (Lausanne, Switzerland) · 2020Review
- Diffuse noxious inhibitory controls and brain networks are modulated in a testosterone-dependent manner in Sprague Dawley rats.Behavioural brain research · 2018Article
- Maternal Separation Induced Visceral Hypersensitivity from Childhood to Adulthood.Journal of neurogastroenterology and motility · 2017Article
- EXPRESS: Histone hyperacetylation modulates spinal type II metabotropic glutamate receptor alleviating stress-induced visceral hypersensitivity in female rats.Molecular pain · 2016Article
- Estrogen modulation of visceral pain.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used functional MRI and a longitudinal design to investigate the brain mechanisms in a previously reported estrogen-dependent visceral hypersensitivity model. We hypothesized that noxious visceral stimulation would be associated with activation of the insula, anterior cingulate cortex, and amygdala, and that estrogen-dependent, stress-induced visceral hypersensitivity would both enhance activation of these regions and recruit activation of other brain areas mediating affect and reward processing. Ovariectomized rats were treated with estrogen (17 β-estradiol, E2) or vehicle (n = 5 per group) and scanned in a 7T MRI at three different time points: pre-stress (baseline), 2 days post-stress, and 18 days post-stress. Stress was induced via a forced-swim paradigm. In a separate group of ovariectomized rats, E2 treatment induced visceral hypersensitivity at the 2 days post-stress time point, and this hypersensitivity returned to baseline at the 18 days post-stress time point. Vehicle-treated rats show no hypersensitivity following stress. During the MRI scans, rats were exposed to noxious colorectal distention. Across groups and time points, noxious visceral stimulation led to activations in the insula, anterior cingulate, and left amygdala, parabrachial nuclei, and cerebellum. A group-by-time interaction was seen in the right amygdala, ventral striatum-pallidum, cerebellum, hippocampus, mediodorsal thalamus, and pontine nuclei. Closer inspection of the data revealed that vehicle-treated rats showed consistent activations and deactivations across time, whereas estrogen-treated animals showed minimal deactivation with noxious visceral stimulation. This unexpected finding suggests that E2 may dramatically alter visceral nociceptive processing in the brain following an acute stressor. This study is the first to examine estrogen-stress dependent interactions in response to noxious visceral stimulation using functional MRI. Future studies that include other control groups and larger sample sizes are needed to fully understand the interactions between sex hormones, stress, and noxious stimulation on brain activity.
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Registered trials
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