Abdominal vagal mediation of the satiety effects of CCK in rats

Roger D. Reidelberger, Jessica Hernandez, Bernd Fritzsch, Martin Hulce

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

CCK type 1 (CCK1) receptor antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCK1 receptors on vagal sensory nerves innervating the small intestine. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of Nα-3-quinolinoyl-D-Glu-N,N-dipentylamide, does not. At dark onset, non-food-deprived control rats and rats with subdiaphragmatic vagotomies received a bolus injection of devazepide (2.5 μmol/kg iv) or a 3-h infusion of A-70104 (3 μmol·kg -1·h-1 iv) either alone or coadministered with a 2-h intragastric infusion of peptone (0.75 or 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. In control rats both antagonists stimulated food intake and attenuated the anorexic response to intragastric infusion of peptone. In contrast, only devazepide was effective in stimulating food intake in vagotomized rats. Thus endogenous CCK appears to act both at CCK1 receptors beyond the blood-brain barrier and by a CCK1 receptor-mediated mechanism involving abdominal vagal nerves to inhibit food intake.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume286
Issue number6 55-6
DOIs
StatePublished - Jun 2004

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Cholecystokinin A Receptor
Devazepide
A 65186
Eating
Blood-Brain Barrier
Peptones
Vagotomy
Small Intestine
Permeability
Salts
Weights and Measures
Food
Injections

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

Abdominal vagal mediation of the satiety effects of CCK in rats. / Reidelberger, Roger D.; Hernandez, Jessica; Fritzsch, Bernd; Hulce, Martin.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 286, No. 6 55-6, 06.2004.

Research output: Contribution to journalArticle

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