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1 Research, VA-NWIHCS, Omaha, NE, USA; Biomedical Sciences, Creighton University, Omaha, NE, USA
2 Research, VA-NWIHCS, Omaha, NE, USA
3 Biomedical Sciences, Creighton University, Omaha, NE, USA
4 Chemistry, Creighton University, Omaha, NE, USA
* To whom correspondence should be addressed. E-mail: roger.reidelberger{at}med.va.gov.
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 N
-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 co-administered 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.
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