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NEUROREGULATION AND MOTILITY

Expression and effects of metabotropic CRF₁ and CRF₂ receptors in rat small intestine

¹Groupe d'Etude du Stress et des Interactions Neuro-Digestives, Equipe d’Accueil 3744, Department of Gastroenterology, Centre Hospitalier Universitaire de Grenoble, Grenoble; and ²Department of Radiobiology and Radiopathology, Centre de Recherches du Service de Santé des Armées, La Tronche, France

Submitted 9 July 2004 ; accepted in final form 4 January 2005

Corticotropin-releasing factor (CRF)-like peptides mediate their effects via two receptor subtypes, CRF₁ and CRF₂; these receptors have functional implication in the motility of the stomach and colon in rats. We evaluated expression and functions of CRF₁ and CRF₂ receptors in the rat small intestine (i.e., duodenum and ileum). CRF_1–2-like immunoreactivity (CRF_1–2-LI) was localized in fibers and neurons of the myenteric and submucosal ganglia. CRF_1–2-LI was found in nerve fibers of the longitudinal and circular muscle layers, in the mucosa, and in mucosal cells. Quantitative RT-PCR showed a stronger expression of CRF₂ than CRF₁ in the ileum, whereas CRF₁ expression was higher than CRF₂ expression in the duodenum. Functional studies showed that CRF-like peptides increased duodenal phasic contractions and reduced ileal contractions. CRF₁ antagonists (CP-154,526 and SSR125543Q) blocked CRF-like peptide-induced activation of duodenal motility but did not block CRF-like peptide-induced inhibition of ileal motility. In contrast, a CRF₂ inhibitor (astressin₂-B) blocked the effects of CRF-like peptides on ileal muscle contractions but did not influence CRF-like peptide-induced activation of duodenal motility. These results demonstrate the presence of CRF_1–2 in the intestine and demonstrate that, in vitro, CRF-like peptides stimulate the contractile activity of the duodenum through CRF₁ receptor while inhibiting phasic contractions of the ileum through CRF₂ receptor. These results strongly suggest that CRF-like peptides play a major role in the regulatory mechanisms that underlie the neural control of small intestinal motility through CRF receptors.

astressin₂-B; corticotropin-releasing factor receptors; urocortin

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