title: Cholecystokinin1 receptors mediate the increase in Fos-like immunoreactivity in the rat myenteric plexus following intestinal oleate infusion.
abstract: Intestinal infusion of nutrients, such as glucose and oleic acid, increase Fos-like immunoreactivity (Fos-LI) in both the enteric nervous system and neurons of the dorsal vagal complex (DVC) of the hindbrain. To test the hypothesis that increased Fos-LI in enteric neurons and the DVC, following intestinal nutrient infusions is mediated by cholecystokinin(1) receptors (CCK(1)), we counted enteric and DVC neurons that expressed Fos-LI following intestinal infusion of oleate or glucose, with and without pretreatment with the CCK(1) receptor antagonist, lorglumide. Both oleate and glucose infusions increased Fos-LI in the DVC. Oleate also increased Fos-LI in the myenteric and submucosal plexuses of the duodenum and the jejunum, but not the ileum, while glucose only increased Fos-LI in the submucosal plexus of the ileum. The CCK(1) receptor antagonist, lorglumide, abolished Fos-LI in the DVC following infusions of either oleate or glucose. In addition, lorglumide attenuated oleate-induced Fos-LI in the myenteric and submucosal plexuses of the duodenum and jejunum. However, lorglumide failed to attenuate glucose-induced Fos-LI in the submucosal plexus of the ileum. These data confirm previous reports indicating that CCK(1) receptors mediate increased DVC Fos-LI following intestinal infusion of oleate or glucose. CCK(1) receptors also contribute to increased Fos-LI in enteric neurons following intestinal oleate infusion. However, failure of lorglumide to attenuate the increase of Fos-LI in the ileal submucosal plexus following intestinal glucose suggests that some intestinal nutrients trigger Fos-LI induction via CCK(1) receptor-independent pathways.
authors.affiliation: Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, AL 36088, USA.
authors.forename: Stephen
authors.initials: S
authors.lastname: Gulley
authors.forename: Mihai
authors.initials: M
authors.lastname: Covasa
authors.forename: Robert C
authors.initials: RC
authors.lastname: Ritter
authors.forename: Ayman I
authors.initials: AI
authors.lastname: Sayegh
mesh_terms: D000818:Animals; D002452:Cell Count / Q000379:methods; D003952:Diagnostic Imaging / Q000379:methods; D004347:Drug Interactions; D006727:Hormone Antagonists / Q000494:pharmacology; D007150:Immunohistochemistry / Q000379:methods; D007422:Intestines / Q000166:cytology / Q000187:drug effects; D008297:Male; D009197:Myenteric Plexus / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D019301:Oleic Acid / Q000008:administration & dosage*; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011949:Receptors, Cholecystokinin / Q000502:physiology*
chemical_list: D006727:Hormone Antagonists; D016760:Proto-Oncogene Proteins c-fos; D011949:Receptors, Cholecystokinin; D019301:Oleic Acid; D011377:Proglumide; C048181:lorglumide