Blockade of brain bombesin/GRP receptors increases food intake in satiated rats

Document Type



Brain and Mind Institute


The mechanisms that initiate or terminate a meal remain obscure. Bombesin (BN) and gene-related peptides (GRP) have been reported to induce a satiety-like state in several species including fowl, mouse, rat, wolf, pig, baboon, and humans. The evolutionary conservation of this pharmacological response suggests a physiological role for the endogenous BN-like peptide(s) in the regulation of food intake. If the release of BN-like peptide(s) represents a "satiety signal" then pharmacological antagonism of this action should enhance food intake and/or postpone satiety. We report herein 1) that [Leu14, psi 13-14]-BN, a BN receptor antagonist, blocks the suppressive effect of centrally administered BN on food intake and 2) that in satiated rats, this pseudopeptide enhances food intake; the effects were more potent and efficacious upon the fourth compared with the third ventricular administration. These results support the contention that endogenous BN-like peptides mediate satiety and that this effect involves brain BN receptors in the caudal brain stem site(s).


This work was published before the author joined Aga Khan University.


The American Journal of Physiology