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Am J Physiol Regul Integr Comp Physiol (November 2, 2006). doi:10.1152/ajpregu.00490.2006
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Submitted on July 12, 2006
Accepted on October 30, 2006

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 rats

Cherese N. Sullivan1, Shannon J Raboin1, Stephen Gulley1, Ntwenzi T. Sinzobahamvya1, Gary M. Green2, Joseph R. Reeve, Jr.3, and Ayman I Sayegh1*

1 Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, Alabama, United States
2 Department of Physiology, University of Texas Health Science Center, San Antonio,, Texas, United States
3 Research Center for Alcoholic Live and Pancreatic Diseases, Veterans Affairs Greater Los Angeles Health Care System and University of California, Los Angeles, California, United States

* To whom correspondence should be addressed. E-mail: sayeghai{at}tuskegee.edu.

We hypothesized that endogenous cholecystokinin 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 non-nutrient releaser of endogenous cholecystokinin (CCK), by orogastric gavage, and Fos-like immunoreactivity (Fos-LI) was quantified in the DVC and the myenteric plexus. The results for endogenous cholecystokinin were compared to 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 cholecystokinin 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 cholecystokinin released by a non-nutrient mechanism requires CCK1 receptors, the vagus nerve, and activation of the DVC, but not the myenteric plexus.




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[Abstract] [Full Text] [PDF]


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