Changes in brain G proteins and colonic sympathetic neural signaling in chronic-acute combined stress @entity35 model of XXXX ( @entity1744 ).

@entity14469 @entity308 @entity697 @entity1109 @entity15342 @entity11026 @entity14 @entity35 @entity1063 @entity1744
The role of the brain-gut axis interaction in the pathogenesis of @entity1744 ( @entity1744 ) is not well understood. To examine this possibility, a novel @entity35 model of @entity1744 subjected to both @entity14469 ( @entity14469 ) was established. G proteins play a crucial role in the pathophysiology of @entity308 . The @entity11026 ( @entity11026 ) and the @entity1063 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 @entity1744 . @entity1109 , and secretion were assessed by counting fecal pellets, abdominal muscle contractions in response to @entity14 ( @entity14 ), 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 @entity15342 induced by @entity14 were significantly higher in both @entity697 ( @entity697 ) and @entity14469 @entity35 . However, the G proteins, @entity11026 , and NET expression changed differently in @entity697 and @entity14469 @entity35 . We showed that exposure to either @entity697 or @entity14469 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 @entity1744 .
