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Dissociation of Locomotor Activation and Suppression of Food Intake Induced by CRF in CRFR1-Deficient Mice

The Scripps Research Institute, Department of Neuropharmacology (A.C., F.D., G.F.K., L.H.G.), and Clayton Foundation Laboratories for Peptide Biology, The Salk Institute (G.W.S., K.F.L., W.V.), La Jolla, California 92037

Address all correspondence and requests for reprints to: Lisa H. Gold, The Scripps Research Institute, Department of Neuropharmacology, 10550 North Torrey Pines Road, La Jolla, California 92037.

	Abstract

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ABSTRACT

Corticotropin-releasing factor (CRF) systems are involved in locomotor and feeding behaviors. Two distinct CRF receptor subtypes, CRFR1 and CRFR2, are thought to mediate CRF actions in the central nervous system. However, the role for each receptor in locomotor activity and feeding remains to be determined. Using CRFR1 null mutant mice, the present study examined the functional significance of this receptor in ambulation and feeding. CRF treatment of wild-type mice resulted in increased levels of locomotion whereas no change was observed in CRFR1-deficient mice as compared to vehicle-treated mutant mice. In contrast, CRF decreased food-water intake in both wild type and CRFR1-deficient mice equally. These results support an important role for CRFR1 in mediating CRF-induced locomotor activation, whereas other receptor subtypes, likely CRFR2, may mediate the appetite-suppressing effects of CRF-like peptides.

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Received March 10, 2000.

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