Bombesin-induced anorexia requires central bombesin receptor activation: independence from interaction with central catecholaminergic systems.

Abstract

Intraperitoneal (IP) administration of bombesin (BBS; 2.5-20 micrograms/kg) induced a dose-dependent inhibition of food intake. The effect was decreased by intraventricular (ICV) administration of bombesin receptor antagonist [Leu14-psi (CH2NH)-Leu13] (3 micrograms/rat) but not by the D1 antagonist SCH 23390, the D2 antagonists sulpiride and pimozide, the dopamine antagonist cis-flupentixol, adrenoceptor blockers phenoxybenzamine or propranolol and serotonergic antagonist methergoline. It is concluded that BBS-induced suppression of feeding may be mediated through central BBS receptors, and is independent of interaction with brain catecholaminergic system.