ArticleNeurogastroenterology and motility2010
Combined administration of secretin and oxytocin inhibits chronic colitis and associated activation of forebrain neurons.
Article in Neurogastroenterology and motility, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Fantastic voyage:Comprehensive psychoneuroendocrinology · 2024Review
- Microbial stimulation of oxytocin release from the intestinal epithelium via secretin signaling.Gut microbes · 2023Article
- Microbial stimulation of oxytocin release from the intestinal epithelium via secretin signaling.bioRxiv : the preprint server for biology · 2023Article
- Effects of secretin gene knockout on the diversity, composition, and function of gut microbiota in adult male mice.Frontiers in cellular and infection microbiology · 2023Article
- Supraspinal Mechanisms of Intestinal Hypersensitivity.Cellular and molecular neurobiology · 2022Review
- Oxytocin and secretin receptors - implications for dry eye syndrome and ocular pain.Frontiers in ophthalmology · 2022Review
- Targeting the Oxytocinergic System: A Possible Pharmacological Strategy for the Treatment of Inflammation Occurring in Different Chronic Diseases.International journal of molecular sciences · 2021Review
- Towards Identifying Genetic Biomarkers for Gastrointestinal Dysfunction in Autism.Journal of autism and developmental disorders · 2020Article
- Intranasal Administration of Oxytocin Attenuates Stress Responses Following Chronic Complicated Stress in Rats.Journal of neurogastroenterology and motility · 2019Article
- Darwin's Other Dilemmas and the Theoretical Roots of Emotional Connection.Frontiers in psychology · 2019Review
- Enteric serotonin and oxytocin: endogenous regulation of severity in a murine model of necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Oxytocin modulates markers of the unfolded protein response in Caco2BB gut cells.Cell stress & chaperones · 2014Article
- Oxytocin modulates mTORC1 pathway in the gut.Biochemical and biophysical research communications · 2013Article
- Anti-stress effects of transcutaneous electrical nerve stimulation (TENS) on colonic motility in rats.Digestive diseases and sciences · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe pathogenesis of inflammatory bowel disease is unknown; however, the disorder is aggravated by psychological stress and is itself psychologically stressful. Chronic intestinal inflammation, moreover, has been reported to activate forebrain neurons. We tested the hypotheses that the chronically inflamed bowel signals to the brain through the vagi and that administration of a combination of secretin (S) and oxytocin (OT) inhibits this signaling.
methodsThree daily enemas containing 2,4,6-trinitrobenzene sulfonic acid (TNBS), which were given to rats produced chronic colitis and ongoing activation of Fos in brain neurons. KEY
resultsFos was induced in neurons in the paraventricular nucleus of the hypothalamus, basolateral amygdala, central amygdala, and piriform cortex. Subdiaphragmatic vagotomy failed to inhibit this activation of Fos, suggesting that colitis activates forebrain neurons independently of the vagi. When administered intravenously, but not when given intracerebroventricularly, in doses that were individually ineffective, combined S/OT prevented colitis-associated activation of central neurons. Strikingly, S/OT decreased inflammatory infiltrates into the colon and colonic expression of tumor necrosis factor-alpha and interferon-gamma. CONCLUSIONS & INFERENCES: These observations suggest that chronic colonic inflammation is ameliorated by the systemic administration of S/OT, which probably explains the parallel ability of systemic S/OT to inhibit the colitis-associated activation of forebrain neurons. It is possible that S and OT, which are endogenous to the colon, might normally combine to restrict the severity of colonic inflammatory responses and that advantage might be taken of this system to develop novel means of treating inflammation-associated intestinal disorders.
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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 OpenQuestion graph.