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neural signaling in chronic-acute combined stress rat model of irritable bowel syndrome (IBS)

 

 

 

 

Transl Res. 2008 Dec;152(6):283-9. Epub 2008 Oct 29.

 

Changes in brain G proteins and colonic sympathetic neural signaling in chronic-acute combined stress rat model of irritable bowel syndrome (IBS).

 

Zou N, Lv H, Li J, Yang N, Xue H, Zhu J, Qian J. Department of Gastroenterology, Peking Union Medical Hospital, Peking Union Medical College & Chinese Academy of Medical Science, Beijing, China, and the Department of Physiology, Capital University of Medical Sciences, Beijing, China.

 

 

The role of the brain-gut axis interaction in the pathogenesis of irritable bowel syndrome (IBS) is not well understood. To examine this possibility, a novel rat model of IBS subjected to both chronic and acute stress (CAS) was established. G proteins play a crucial role in the pathophysiology of depression. The alpha 2A adrenoceptor (alpha(2A)-AR) and the norepinephrine reuptake transporter (NET) determine the sympathetic signal activity. It is conceivable that stress may induce brain G proteins, colonic alpha(2A)-ARs, and NET abnormal expression, which may be responsible for the abnormalities in IBS. Colonic motility, visceral sensation, and secretion were assessed by counting fecal pellets, abdominal muscle contractions in response to colorectal balloon distension (CRD), and short-circuit current study, respectively. Western blot analysis was used to investigate the expression of G proteins, alpha(2A)-ARs, and NET. Compared with control animals, the colonic epithelial secretion, fecal pellets, and numbers of abdominal muscle contraction induced by CRD were significantly higher in both acute stress only (AS) and CAS rats. However, the G proteins, alpha(2A)-AR, and NET expression changed differently in AS and CAS rats. We showed that exposure to either AS or CAS would cause the increase of secretion, motility, and sensation, but the change of protein expression in brain-gut axis was different. It may be responsible for the pathogenesis of IBS.

 

PMID: 19059163 [PubMed - in process]

 

 

 

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