Several mammalian avian species, including the chicken, show migrating myoelectric complexes (MMC) both in unfed and fed states. In these species, postprandial hormones seem to modulate but not to disrupt the MMC. To gain more information in this modulatory role, we evaluated the role of cholecystokinin (CCK) vs gastrin on the regulation of intestinal motility in chickens. Birds were implanted with eight electrodes for electromyography in the stomach, duodenum, jejunum, and ileum. In feed-deprived animals, CCK infusion (10(-12) mol/kg per min x 3 h) did not disrupt the MMC but induced changes in the MMC pattern similar to those induced by a meal. Infusion of CCK in fed animals induced dose-dependent effects: CCK infused at 10(-11) and 3 x 10(-11) mol/kg per min x 2 h, progressively elongated the MMC and slowed the speed of propagation of Phase 3. Furthermore, CCK infused at 10(-10) mol/kg per min x 2 h disrupted the MMC but a Phase 3 appeared just after the end of the infusion. By contrast, chicken gastrin (10(-10) mol/kg per min x 2 h) did not modify the MMC pattern. In conclusion, CCK influence on the intestinal motility of chickens ranges from the modulation of the MMC to total disruption, depending on the dose. Moreover, this study suggests that the mechanism of action of CCK could be similar in both mammalian and avian small intestines.