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1 Surgery, Duke University, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: ttakahas{at}duke.edu.
CRF (corticotropin releasing factor) is one of the most important factors to the mechanism of stress-induced stimulation of colonic motility. However, it is controversial whether stress-induced stimulation of colonic motility is mediated via central or peripheral CRF receptors. We investigated the hypothesis that peripherally injected CRF accelerate colonic motility through central CRF receptor, but not peripheral CRF receptor. A strain gauge transducer was sutured on the serosal surface of the proximal colon. Colonic motility was monitored before and after the peripheral injection of CRF. In vitro muscle strip study was also performed to investigate the peripheral effects of CRF. Subcutaneous injection of CRF (30-100 µg/kg) stimulated colonic motility in a dose-dependent manner. The stimulatory effect of peripherally administered CRF on colonic motility was abolished by truncal vagotomy, hexamethonium, atropine, and intracisternal (IC) injection of astressin (a CRF receptor antagonist). No responses were observed to CRF (10-9 M -10-7 M) of the muscle strips of the proximal colon. These results suggested that the stimulatory effect of colonic motility in response to peripheral administration of CRF is mediated by vagus nerve, nicotinic receptors, muscarinic receptors and CRF receptors of the brain stem. It is concluded that peripherally administered CRF reaches area postrema and activates dorsal nucleus of vagi (DMV) via central CRF receptors, resulting in stimulation of vagal efferent and cholinergic transmission of the proximal colon.
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