Bilateral midbrain transections block the behavioral effects of cholecystokinin on feeding and exploration in rats.

The mechanism by which peripherally administered cholecystokinin (CCK) reduces feeding and exploration involves a sensory feedback pathway from the gastrointestinal regions, via the vagus nerve through the nucleus tractus solitarius (NTS). Bilateral dorsal midbrain transections rostral to the NTS abolish the ability of CCK to reduce food consumption, decrease exploratory approaches, and increase pauses of behavioral inactivity, as compared to these actions of CCK in normal and sham-lesioned control rats, suggesting that ascending NTS fibers are a necessary component in this feedback system.