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Articles in PresS, published online ahead of print October 30, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00292.2001
Submitted on July 5, 2001
Accepted on October 21, 2002
1 Department of Anatomy, Physiology and Cell Biology, UC Davis School of Veteriniary Medicine, Davis, CA, USA
2 CURE Digestive Diseases Research Center, Department of Medicine, UCLA School of Medicine, Los Angeles, CA, USA; VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA
3 CURE Digestive Diseases Research Center, Department of Medicine, UCLA School of Medicine, Los Angeles, CA, USA
4 CURE Digestive Diseases Research Center, Department of Medicine, UCLA School of Medicine, Los Angeles, CA, USA; Department of Neurobiology, UCLA School of Medicine, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: heraybould{at}ucdavis.edu.
Intestinal perfusion with carbohydrate inhibits gastric emptying via vagal and spinal capsaicin-sensitive afferent pathways. The aim of the present study was to determine (1) the role of 5-HT3 receptors (5-HT3R) in mediating glucose-induced inhibition of gastric emptying and (2) 5-HT3R expression in vagal and spinal afferents 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/Kg H2O). 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 C-terminal of the rat 5-HT3R, was found in over 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.
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