Neurochemical investigation of the afferent pathway from the vagus nerve to the nucleus tractus solitarius in mediating the "satiety syndrome" induced by systemic cholecystokinin.

The satiety syndrome induced by intraperitoneally administered cholecystokinin (CCK) requires an intact visceral sensory feedback system involving the afferent vagus nerve and the nucleus tractus solitarius (NTS). Since both the vagus and the NTS contain CCK, the vagal-NTS synapse could conceivably employ CCK as a transmitter. To test this hypothesis, CCK was injected directly into the NTS region in awake rats. CCK at doses of 1 ng, 10 ng, and 100 ng had no effect on food consumption or exploratory behaviors associated with the satiety syndrome. The acetylcholine agonist carbachol, injected directly into the NTS region, effectively mimicked the actions of intraperitoneally administered CCK on feeding and exploration. These data suggest that CCK is not the transmitter at the vagal-NTS site in the visceral sensory pathway projecting to brain regions mediating the reduced feeding and exploration actions of systemic CCK.