Lesion of vagal afferent terminals impairs glucagon-induced suppression of food intake.

Selective hepatic branch vagotomy impairs glucagon-induced inhibition of food intake. However, the relative importance of afferent and efferent neurons in glucagon satiety has not been directly investigated. In this experiment, lesions were placed in the area postrema (AP) and immediately subjacent nucleus of the solitary tract (NTS) where hepatic vagal afferents have been reported to terminate. We found that these lesions impaired glucagon-induced satiety under testing conditions similar to those that reveal a glucagon satiety deficit in rats with selective hepatic branch vagotomies. Since these lesions did not damage the underlying dorsal motor nucleus of the vagus, our results suggest that our AP/NTS lesions impaired glucagon satiety by damaging terminal fields of vagal afferent neurons. Finally, our lesions did not impair satiety induced by cholecystokinin (CCK), a response mediated by gastric vagal afferent neurons. This latter result suggests that the vagal afferent terminal fields required for glucagon- and CCK-induced satiety are not coextensive.