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Received December 13, 2003
Revised January 20, 2004
Accepted after revision January 26, 2004
1 AstraZeneca R&D Mölndal
2 CURE: Digestive Diseases Research Center
3 Salk Institute for Biological Studies
4 Neurocrine Biosciences
5 University of California at Los Angeles
* To whom correspondence should be addressed. E-mail: ytache{at}ucla.edu.
Recently characterized selective agonists and developed antagonists for the corticotropin releasing factor (CRF) receptors provide new tools to investigate stress-related functional changes. The influence of mammalian CRF and related peptides injected intracerebroventricularly (i.c.v.) on gastric and colonic motility, the CRF receptor subtypes involved and their role in colonic response to stress were studied in conscious mice. The CRF1/CRF2 agonists, rat urocortin 1 (rUcn 1) and rat/human (r/h)CRF, the preferential CRF1 agonist, ovine (o)CRF, and the CRF2 agonist, mouse (m)Ucn 2, injected i.c.v. inhibited gastric emptying and stimulated distal colonic motor function (bead transit and defecation) while oCRF9-33OH (devoid of CRF receptor affinity) showed neither effects. mUcn 2 injected peripherally had no colonic effect. The selective CRF2 antagonist, astressin2-B (i.c.v.), at 20:1 antagonist:agonist ratio blocked i.c.v. r/hCRF and rUcn 1 induced inhibition of gastric transit and reduced that of mUcn 2 while the CRF1 antagonist, NBI-35965, had no effect. By contrast, the colonic motor stimulation induced by i.c.v. r/hCRF and rUcn 1, and 1 h restraint stress were antagonized only by NBI-35965 while both that of mUcn 2 was equally blocked by both antagonists. None of the antagonists injected i.c.v. alone influenced gut transit. These data establish in mice that brain CRF1 receptors mediate the stimulation of colonic transit induced by central CRF, urocortins (1 and 2) and restraint stress, while CRF2 receptors mediate the inhibitory actions of these peptides on gastric transit.
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