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Hindbrain GRP receptor blockade antagonizes feeding suppression by peripherally administered GRP
E E Ladenheim1, J E Taylor, D H Coy
1Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
The American Journal of Physiology
|July 1, 1996
Summary
Bombesin-like peptides reduce food intake. Blocking gastrin-releasing peptide (GRP) receptors in the hindbrain prevents peripheral GRP from suppressing glucose intake in rats, showing central GRP receptor involvement.
Area of Science:
- Neuroscience
- Endocrinology
- Behavioral Science
Background:
- Bombesin (BN)-like peptides are known to suppress food intake through both central and peripheral administration routes.
- The caudal hindbrain is implicated as a critical site for mediating the feeding effects of BN-like peptides.
- The precise relationship between central and peripheral actions of BN on feeding remains unclear.
Purpose of the Study:
- To investigate the necessity of caudal hindbrain gastrin-releasing peptide (GRP) receptors for the food intake-suppressing effects of peripherally administered GRP.
- To determine if blocking central GRP receptors affects peripheral GRP's ability to suppress glucose intake.
Main Methods:
- Male Sprague-Dawley rats, food-deprived for 5 hours, were used.
- Intraperitoneal administration of GRP-(18-27) was used to suppress glucose intake.
- Fourth ventricular infusion of a specific GRP antagonist, [D-F5, Phe6, D-Ala11]BN-(6-13) methyl ester (BN-ME), was employed to block central GRP receptors.
Main Results:
- Fourth ventricular administration of BN-ME dose-dependently blocked the suppression of glucose intake induced by peripheral GRP-(18-27).
- The highest dose of BN-ME (100 ng) completely inhibited the effect of peripheral GRP-(18-27) on glucose intake.
- BN-ME alone, when infused into the fourth ventricle, did not alter glucose intake, indicating its specificity as a blocking agent.
Conclusions:
- The findings demonstrate that caudal hindbrain GRP receptors are essential for the anorectic effects of peripherally administered GRP-(18-27).
- This study highlights the critical role of central GRP receptor signaling in mediating the peripheral actions of GRP on food intake regulation.
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