Ablation of the ventral portion of nucleus medianus (vNM) in rats produced a temporary adipsia or hypodipsia that was accompanied by pronounced urinary fluid losses. When ad libitum drinking resumed, about half of the brain-damaged animals became hyperdipsic, exhibiting chronic two- to threefold elevations in their daily water intakes during the nocturnal hours of the day-night cycle. Rats that remained normodipsic after vNM ablation usually exhibited hyperdipsia if they were food-deprived overnight. The basis for the hyperdipsia produced by vNM ablation was not clear. The elevated water intakes appeared not to result from chronic urinary fluid losses, because hyperdipsic rats were able to concentrate their urine during the day, when they drank little. Moreover, the animals did not seem to be volume depleted; their plasma renin activities were not elevated, and they drank normally in association with meals. These and other findings suggest that vNM lesions damage neural substrates that control drinking behavior, and the hyperdipsia results from this rather than from physiological changes produced by the lesion.