4.2 Article

Mechanisms of Stress-Induced Visceral Pain: Implications in Irritable Bowel Syndrome

期刊

JOURNAL OF NEUROENDOCRINOLOGY
卷 28, 期 8, 页码 -

出版社

WILEY
DOI: 10.1111/jne.12361

关键词

irritable bowel syndrome; visceral hypersensitivity; stress; amygdala; corticotrophin-releasing hormone; mucosal immunity

资金

  1. Department of Veterans Affairs, USA
  2. Presbyterian Health Foundation, Oklahoma City, OK USA
  3. ISPNE
  4. Department of Veterans Affairs [VA BX-10-007, BX-001195-05]
  5. Presbyterian Health Foundation Endowed Chair in Neurosciences
  6. Fondo de Investigacion Sanitaria
  7. Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBERehd)
  8. Instituto de Salud Carlos III
  9. Subdireccion General de Investigacion Sanitaria
  10. Ministerio de Economia y Competitividad [CP10/00502 PI13/00935, CB06/04/0021]

向作者/读者索取更多资源

Visceral pain is a term describing pain originating from the internal organs of the body and is a common feature of many disorders, including irritable bowel syndrome (IBS). Stress is implicated in the development and exacerbation of many visceral pain disorders. Recent evidence suggests that stress and the gut microbiota can interact through complementary or opposing factors to influence visceral nociceptive behaviours. The Young Investigator Forum at the International Society of Psychoneuroendocrinology (ISPNE) annual meeting reported experimental evidence suggesting the gut microbiota can affect the stress response to affect visceral pain. Building upon human imaging data showing abnormalities in the central processing of visceral stimuli in patients with IBS and knowledge that the amygdala plays a pivotal role in facilitating the stress axis, the latest experimental evidence supporting amygdala-mediated mechanisms in stress-induced visceral pain was reviewed. The final part of the session at ISPNE reviewed experimental evidence suggesting that visceral pain in IBS may be a result, at least in part, of afferent nerve sensitisation following increases in epithelial permeability and mucosal immune activation.

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