Rats received electrolytic lesions centered in the gustatory subnucleus of the ventral posterior complex of the thalamus. They were tested for impairments of the ability to increase sodium chloride intake after depletion of body sodium or treatment with the mineralocorticoid desoxycorticosterone. Tests were administered either within a few weeks or after 2 months postoperative recovery to test a hypothesis suggested by previous studies that the decremental effect of the lesions would appear only after a latent period. This hypothesis was refuted by the results-the thalamic lesions resulted in highly significant impairments of sodium intake at either time period. An additional finding was that a particular type of general feeding impairment previously attributed to subthalamic damage also occurs after thalamic lesions.