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This Article Full Text Full Text (PDF) All Versions of this Article: 293/2/G493    most recent 00118.2007v1 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 Viard, E. Articles by Travagli, R. A. Search for Related Content PubMed PubMed Citation Articles by Viard, E. Articles by Travagli, R. A.

NEUROREGULATION AND MOTILITY

Vagally mediated, nonparacrine effects of cholecystokinin-8s on rat pancreatic exocrine secretion

¹Department of Neuroscience, Pennington Biomedical Research Center-Louisiana State University System, Baton Rouge, Louisiana; and ²Key Laboratory of Allergy and Immune-Related Diseases-Department of Physiology, School of Basic Medical Science, Wuhan University, Wuhan, Hubei, People's Republic of China

Submitted 7 March 2007 ; accepted in final form 12 June 2007

Cholecystokinin (CCK) has been proposed to act in a vagally dependent manner to increase pancreatic exocrine secretion via actions exclusively at peripheral vagal afferent fibers. Recent evidence, however, suggests the CCK-8s may also affect brain stem structures directly. We used an in vivo preparation with the aims of 1) investigating whether the actions of intraduodenal casein perfusion to increase pancreatic protein secretion also involved direct actions of CCK at the level of the brain stem and, if so, 2) determining whether, in the absence of vagal afferent inputs, CCK-8s applied to the dorsal vagal complex (DVC) can also modulate pancreatic exocrine secretion (PES). Sprague-Dawley rats (250–400 g) were anesthetized and the common bile-pancreatic duct was cannulated to collect PES. Both vagal deafferentation and pretreatment with the CCK-A antagonist lorglumide on the floor of the fourth ventricle decreased the casein-induced increase in PES output. CCK-8s microinjection (450 pmol) in the DVC significantly increased PES; the increase was larger when CCK-8s was injected in the left side of the DVC. Protein secretion returned to baseline levels within 30 min. Microinjection of CCK-8s increased PES (although to a lower extent) also in rats that underwent complete vagal deafferentation. These data indicate that, as well as activating peripheral vagal afferents, CCK-8s increases pancreatic exocrine secretion via an action in the DVC. Our data suggest that the CCK-8s-induced increases in PES are due mainly to a paracrine effect of CCK; however, a relevant portion of the effects of CCK is due also to an effect of the peptide on brain stem vagal circuits.

brain stem; dorsal vagal complex; exocrine pancreas

This article has been cited by other articles:

				G. M. Holmes, M. Tong, and R. A. Travagli Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex Am J Physiol Gastrointest Liver Physiol, March 1, 2009; 296(3): G621 - G631. [Abstract] [Full Text] [PDF]