Antagonistic effects of naloxone on CCK-octapeptide induced satiety and rumino-reticular hypomotility in sheep.

Continuous intracerebroventricular (ICV) infusion of CCK-octapeptide (CCK8) was performed in ewes fitted with a permanent cannula into the lateral cerebral ventricle and Nichrome electrodes on the reticulum in order to record its electrical activity. In the first series of experiments, subsequently repeated in 12 h fasted animals, CCK8 was infused during the first hour of a 3 hour period of feeding at 2.5, 5 and 10 ng.kg-1.min-1. The same series of infusion were performed 20 min after ICV injection of 2.4 and 10 micrograms.kg-1 of naloxone. CCK8 reduced significantly in a dose related manner the food intake (r = 0.95; P less than 0.01) and the frequency of cyclic spike bursts associated to biphasic contractions of the reticulum observed during feeding (r = 0.89; P less than 0.01). At 5 and 10 ng.kg-1.min-1, the reduction of food intake reached 46.2 and 52.6% during the period of infusion; the basal and stimulated (feeding) frequency of reticular contractions were nearly halved. Previous ICV administration of naloxone (2.4 micrograms.kg-1) partially blocked the effects of CCK8 infusion on both food intake (72%) and reticular frequency (54% basal, 67% stimulated). The CCK8 induced effects on both food intake and frequency of reticular contraction were completely abolished after a previous 10 micrograms.kg-1 injection of naloxone. These results suggest that the central effects of CCK8 on feeding behavior and forestomach motility involve similar central structures and are mediated through opiate receptor structures.