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1 Research Service, Department of Veterans Affairs Nebraska Western Iowa Health Care System, Omaha, NE, USA; Department of Biomedical Sciences, Creighton University, Omaha, NE, USA
2 Department of Chemistry, Creighton University, Omaha, NE, USA
* To whom correspondence should be addressed. E-mail: roger.reidelberger{at}med.va.gov.
Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated in part by CCK action at CCKARs located peripheral to the blood-brain barrier. At dark onset, non-food-deprived rats received a bolus injection of devazepide (2.5 µmol/kg iv), a 3-h infusion of A-70104 (1 or 3 µmol kg-1 h-1 iv), or vehicle either alone or co-administered with a 3-h infusion of CCK-8 (10 nmol kg-1 h-1 iv) or a 2-h intragastric infusion of peptone (1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of N
-3-quinolinoyl-D-Glu-N,N-dipentylamide (A-65186), does not. CCK-8 inhibited 3-h food intake by more than 50% and both A-70104 and devazepide abolished this response. A-70104 and devazepide stimulated food intake and similarly attenuated the anorexic response to intragastric infusion of peptone. Thus, endogenous CCK appears to act in part at CCKARs peripheral to the blood-brain barrier to inhibit food intake.
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