title: Postprandial neuronal activation in the nucleus of the solitary tract is partly mediated by CCK-A receptors.
abstract: CCK-A receptors and neurons of the nucleus of the solitary tract (NTS) are involved in the regulation of food intake, and in rats, there is evidence for involvement of an intestinal vagal afferent pathway. Studies investigating the role of CCK-A receptors in activation of NTS neurons using highly selective CCK-A receptor agonists and antagonists have yielded conflicting data. In the present study, we investigated CCK-induced and postprandial activation of NTS neurons, together with food intake studies, in CCK-A receptor-deficient Otsuka Long-Evans Tokushima fatty (OLETF) rats. Activated NTS neurons were detected using immunohistological staining for c-Fos protein. Exogenous CCK increased the number of c-Fos protein-positive cells in the NTS of Sprague-Dawley and CCK-A receptor-intact Long-Evans Tokushima Otsuka (LETO) rats but had no effect in CCK-A receptor-deficient OLETF rats. Food intake-induced c-Fos protein expression in NTS neurons was significantly reduced in CCK-A receptor-deficient OLETF rats compared with Sprague-Dawley or LETO rats. Postprandial c-Fos protein expression in the NTS was also significantly decreased after pretreatment with the CCK-A receptor antagonist MK329 after both short- and long-term fasting periods. Exogenous CCK decreased cumulative food intake in Sprague-Dawley and LETO rats but not in OLETF rats. These data demonstrate that CCK-A receptors are involved in the CCK- and food-induced c-Fos protein expression in the NTS. Taken together with the results of the food intake studies, this suggests that activation of CCK-A receptors is involved in the postprandial activation of NTS neurons and in the regulation of food intake.
authors.affiliation: University Hospital, Department of General and Transplantation Surgery, University of Tübingen, 72076 Tübingen, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Glatzle
authors.forename: M E
authors.initials: ME
authors.lastname: Kreis
authors.forename: K
authors.initials: K
authors.lastname: Kawano
authors.forename: H E
authors.initials: HE
authors.lastname: Raybould
authors.forename: T T
authors.initials: TT
authors.lastname: Zittel
mesh_terms: D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology; D001786:Blood Glucose; D002766:Cholecystokinin / Q000494:pharmacology; D020109:Devazepide / Q000494:pharmacology; D004435:Eating / Q000187:drug effects / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000502:physiology*; D010671:Phenylurea Compounds / Q000494:pharmacology; D019518:Postprandial Period / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D020334:Rats, Inbred OLETF; D017207:Rats, Sprague-Dawley; D043886:Receptor, Cholecystokinin A; D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012527:Satiation / Q000502:physiology; D017552:Solitary Nucleus / Q000166:cytology / Q000502:physiology*
chemical_list: D001570:Benzodiazepinones; D001786:Blood Glucose; D006727:Hormone Antagonists; D010671:Phenylurea Compounds; D016760:Proto-Oncogene Proteins c-fos; D043886:Receptor, Cholecystokinin A; D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin; C058121:L 365260; D002766:Cholecystokinin; D020109:Devazepide