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This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/R1071    most recent 00490.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Sullivan, C. N. Articles by Sayegh, A. I. Search for Related Content PubMed PubMed Citation Articles by Sullivan, C. N. Articles by Sayegh, A. I.

APPETITE, OBESITY, DIGESTION, AND METABOLISM

Endogenous cholecystokinin reduces food intake and increases Fos-like immunoreactivity in the dorsal vagal complex but not in the myenteric plexus by CCK₁ receptor in the adult rat

¹Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, Alabama; ²Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas; and ³CURE: Digestive Diseases Research Center, Veterans Administration Greater Los Angeles Healthcare System, and Digestive Diseases Division, School of Medicine, University of California, Los Angeles California

Submitted 12 July 2006 ; accepted in final form 30 October 2006

We hypothesized that endogenous CCK reduces food intake by activating the dorsal vagal complex (DVC) and the myenteric neurons of the gut. To test this hypothesis, adult rats were given camostat mesilate; a nonnutrient releaser of endogenous CCK, by orogastric gavage, and Fos-like immunoreactivity (Fos-LI) was quantified in the DVC and the myenteric plexus. The results for endogenous CCK were compared with those for exogenous CCK-8. Exogenous CCK-8 reduced food intake and stimulated Fos-LI in the DVC and in myenteric neurons of the duodenum and jejunum. In comparison, endogenous CCK reduced food intake and increased DVC Fos-LI but did not increase Fos-LI in the myenteric plexus. Similar to CCK-8, devazepide, a specific CCK₁ receptor antagonist, and not L365,260, a specific CCK₂ receptor antagonist, attenuated the reduction of food intake by camostat. In addition, Fos-LI in the DVC in response to both exogenous CCK-8 and camostat administration was significantly attenuated by vagotomy, as well as by blocking CCK₁ receptors. These results demonstrate for the first time that reduction of food intake in adult rats by endogenous CCK released by a nonnutrient mechanism requires CCK₁ receptors, the vagus nerve, and activation of the DVC, but not the myenteric plexus.

camostat; vagotomy; devazepide

This article has been cited by other articles:

				S. V. Wu, K. G. Harikumar, R. J. Burgess, J. R. Reeve Jr., and L. J. Miller Effects of cholecystokinin-58 on type 1 cholecystokinin receptor function and regulation Am J Physiol Gastrointest Liver Physiol, September 1, 2008; 295(3): G641 - G647. [Abstract] [Full Text] [PDF]