Unit activity from neurons of hypothalamic feeding and satiety mechanisms, and from adjacent hypothalamic regions was recorded in anesthetized dogs with surgically exposed hypothalamus, and in Flaxedil-immobilized cats in which a stereotaxic approach was made. Intravenous glucose or insulin, or combinations of both, were given and the changes in spike activity observed. Glucose estimations were done on blood samples taken from femoral artery and vein. In starved animals the unit activity in satiety center neurons was slower than that obtained from feeding center neurons. Frequency of spikes recorded from satiety center neurons increased and that of feeding center neurons decreased significantly after glucose was given intravenously, while spike activity from these centers showed a reverse pattern of response after intravenous insulin. No significant changes were observed from other hypothalamic and cortical neurons. Activity of neurons of the satiety center did not show a significant correlation with blood glucose level per se, but a better correlation was found between unit activity and the A-V glucose difference. It is suggested that the satiety center is activated by increased glucose utilization in the body.