Microinfusion of 5-thioglucose into either the lateral or fourth cerebral ventricle caused increased feeding and hyperglycemia in rats when the cerebral aqueduct was unobstructed. If the aqueduct was obstructed and 5-thioglucose was infused into the fourth ventricle, increased feeding and hyperglycemia persisted, whereas feeding and hyperglycemia in response to lateral ventricle infusion were abolished. Drinking in response to infusion of angiotensin II into the lateral ventricle was not diminished by aqueduct obstruction. These results indicate that glucoreceptors that mediate feeding and hyperglycemia in response to cerebral glucoprivation are located in the caudal hindbrain and not in the hypothalamus where they have previously been sought.