Dorsomedial hindbrain participation in cholecystokinin-induced satiety.

To study the role of the dorsomedial hindbrain in cholecystokinin (CCK)-induced satiety, lesions were produced in the region of the obex. We observed that lesions that were limited to the area postrema (AP) and immediately adjacent nucleus of the solitary tract (NST) did not attenuate the satietogenic effects of CCK. Similarly, lesions of the medial NST rostral to the AP had no effect on CCK-induced satiety. However, when the majority of the medial and commissural subnuclei of the NST as well as the AP were lesioned, there was a significant attenuation of the satietogenic effect of CCK. Since this lesion includes the bulk of the terminal field from the gastric branch of the vagus nerve, these results support the role of gastric afferent projections in the mediation of CCK-induced satiety. Although we do not rule out the possibility that the AP itself monitors circulating CCK, our data clearly show that the AP is not essential for induction of satiety by exogenous CCK.