Postprandial cholecystokinin (CCK) has been suggested as an important mediator of disruption of migrating myoelectric complexes (MMC) after a meal. However, the role of CCK in regulating small intestinal motility in rats and the participation of central and/or peripheral CCK-A and B receptors in CCK actions, are still unclear. For this study, Sprague-Dawley rats were prepared with electrodes in the small intestine, a catheter in the jugular vein and an intracerebroventricular (i.c.v.) cannula. Postprandial disruption of the MMC was blocked by the i.v. infusion of the CCK-B antagonist L-365,260 (2 x 10(-7) mol/kg), but not by the infusion of the CCK-A antagonist L-364,718. When administered i.c.v., L-364,718 (2.25 x 10(-9) mol), but not L-365,260, restored the MMC pattern. The i.v. infusion of CCK-8 (1-3 x 10(-9) mol/kg) or CCK-4 (10(-7) mol/kg) disrupted the MMC pattern. CCK-8 effects where prevented by the i.v. infusion of either L-364,718 or L-365,260. Administered i.c.v., only the antagonist L-364,718 prevented CCK-8 disruption of the MMC. These results suggest that CCK-mediated motor changes after a meal are due to stimulation of peripheral CCK-B receptors. CCK also induces a release of central CCK that through CCK-A receptors participates on MMC disruption.