Rats with complete subdiaphragmatic bilateral transection of the abdominal vagus (Vgx-C) showed disordered food-related drinking when drinking water in temporal association with a meal of dry food after 5-hr food deprivation and when drinking water in association with a liquid meal after 24-hr food deprivation. The Vgx-C rats drank after significantly longer latencies and drank significantly less water in 1 hr than did sham-vagotomized (Sham) rats after eating the same size meal (solid or liquid) as Shams. Rats with incomplete vagal transection (Vgx-I) ate and drank like Shams. Water intake of Sham and Vgx-I rats correlated positively with the meal size of solid food, but the water intake of Vgx-C rats did not. The failure of Vgx-C rats to drink water normally when food was ingested was not due to failure of a food stimulus to reach the intestine, because Vgx-C and Sham rats emptied equivalent volumes of liquid food from the stomach into the intestine within 10 min of food entering the stomach. These results indicate that the abdominal vagus is an important neurological substrate for food-related drinking in the rat.

After 3-hr food deprivation, rats with gastric fistulas ate liquid food with the fistula closed (normal feeding) or open (sham feeding). Meal size (MS) was larger, latency to rest (LR) after a meal was longer, and intermeal interval (IMI) was shorter during sham feeding than during normal feeding. The putative satiety signal cholecystokinin (CCK, 20% pure) decreased MS and LR and increased IMI during sham feeding. After CCK (30 U/kg) the MS, LR, and IMI were the same during sham feeding as during normal feeding. The synthetic octapeptide (OCT) of CCK, which has the known biological actions of the complete hormone, reproduced the effects of CCK (30 U/kg) on MS and LR but not on IMI. Ingestive behavior was not nonspecifically suppressed by CCK or OCT because water drinking was not inhibited by CCK or OCT. The CCK and OCT were also tested for their ability to serve as unconditioned stimuli (UCS) for the formation of a conditioned taste aversion (CTA) in the 3-hr food-deprived sham-feeding rat. The OCT (30 U/kg) did not serve as a UCS for a CTA in the same sham-feeding conditions in which OCT produced normal MS and LR. Impure CCK (30 U/kg), however, did serve as a UCS for a CTA under these conditions. The differential effectiveness of CCK and OCT for IMI and CTA may be due to non-CCK factors in the impure extract of CCK. These experiments demonstrate that the preabsorptive food-contingent stimuli of sham feeding plus exogenous CCK are sufficient for normal short-term satiety under certain conditions, and they provide further evidence consistent with the hypothesis that cholecystokinin produces satiety in rats.

After 3 hr food deprivation, rats with gastric fistulas ate liquid food with the fistula closed (normal feeding) or open (sham feeding). On the first sham feeding test, meal size (MS) was larger and intermeal interval (IMI) was shorter than during normal feeding. The collection of ingested food and phenol red labelled diet through the fistula was complete during sham feeding under these conditions. These experiments show that pregastric food-contingent stimuli -alone (sham feeding) are sufficient for the termination of a meal, appearance of postprandial resting behavior and for a measurable IMI under conditions resembling those of normal feeding for laboratory rats in the light phase of a diurnal cycle. Pregastric stimuli alone are not sufficient for normal satiety, however, because sham-fed MS is larger and IMI is shorter than normal. This sham feeding paradigm may serve as a useful behavioral assay for postprandial satiety.