Hindbrain grp receptor blockade antagonizes feeding suppression by
peripherally administered grp.
Ladenheim, Ellen E., John E. Taylor, David H. Coy, Kimberly A. Moore,
and Timothy H. Moran.
Department of Psychiatry and Behavioral Sciences, The Johns Hopkins
University School of Medicine, Baltimore, MD 21205, Biomeasure, Inc,
27 Maple Street, Milford, MA 01757, Peptide Research Laboratories,
Department of Medicine, Tulane University Medical Center, New
Orleans, LA 70112
APStracts 3:0084R, 1996.
Bombesin (BN)-like peptides injected peripherally or centrally
suppress food intake in rats. The relationship between the central
and peripheral actions of BN is unknown. However, experimental
evidence supports a critical role for the caudal hindbrain in
mediating BN's feeding effects. To investigate this relationship
further, we examined the ability of fourth ventricular infusion of a
specific gastrin-releasing peptide (GRP) antagonist, [D-F5,Phe6,D
-Ala11]BN(6-13)methyl ester (BN-ME) to block suppression of glucose
intake (0.5 kcal/ml) produced by intraperitoneal administration of
GRP18-27 in 5 h food-deprived male Sprague-Dawley rats (n=10). We
found that fourth ventricular administration of 10, 32 and 100 ng BN
-ME blocked the suppression of glucose intake produced by peripherally
administered 10 nmol/kg GRP18-27. The most effective dose of BN-ME
(100 ng) blocked the ability of peripheral injection of GRP18-27 to
inhibit glucose intake but had no effect on intake when given alone.
These results demonstrate that the availability of caudal hindbrain
GRP receptors is necessary for peripherally administered GRP18-27 to
reduce food intake in rats.
Received 28 September 1995; accepted in final form 14 February
1996.
APS Manuscript Number R614-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96