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1 Department of Anatomy, Physiology and Cell Biology, University of California Davis School of Veterinary Medicine, Davis 95616; and CURE Digestive Diseases Research Center, Veterans Affairs Greater Los Angeles Healthcare System, Division of Digestive Diseases, Departments of 2 Medicine and 3 Neurobiology, University of California Los Angeles School of Medicine, Los Angeles, California 95616
Intestinal perfusion with carbohydrates inhibits gastric emptying via vagal and spinal capsaicin-sensitive afferent pathways. The aim of the present study was to determine the role of 1) 5-hydroxytryptamine (5-HT)3 receptors (5-HT3R) in mediating glucose-induced inhibition of gastric emptying and 2) 5-HT3R expression in vagal and spinal afferents in innervating the duodenum. In awake rats fitted with gastric and duodenal cannulas, perfusion of the duodenum with glucose (50 and 100 mg) inhibited gastric emptying. Intestinal perfusion of mannitol inhibited gastric emptying only at the highest concentration (990 mosm/kgH2O). Pretreatment with the 5-HT3R antagonist tropisetron abolished both glucose- and mannitol-induced inhibition of gastric emptying. Retrograde labeling of visceral afferents by injection of dextran-conjugated Texas Red into the duodenal wall was used to identify extrinsic primary afferents. Immunoreactivity for 5-HT3R, visualized with an antibody directed to the COOH terminus of the rat 5-HT3R, was found in >80% of duodenal vagal and spinal afferents. These results show that duodenal extrinsic afferents express 5-HT3R and that the receptor mediates specific glucose-induced inhibition of gastric emptying. These findings support the hypothesis that enterochromaffin cells in the intestinal mucosa release 5-HT in response to glucose, which activates 5-HT3R on afferent nerve terminals to evoke reflex changes in gastric motility. The primary glucose sensors of the intestine may be mucosal enterochromaffin cells.
glucose; carbohydrate; monosaccharide; enterochromaffin cells; 5-hydroxytryptamine
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