Three nanomoles of kainic acid (KA) was injected into the striatum of rats to produce selective lesions in striatal neurons. Postoperatively the rats with lesions showed temporary aphagia and adipsia, and their mean body weight was reduced compared to sham-operated controls. Although a significant difference in body weight was maintained throughout the experiments, no significant differences were observed in ad libitum water or food intake between the animals recovered from lesions and the control animals. When the rats with striatal lesions were deprived of food for 24 h their water intake was substantially greater than that of control rats. Twenty-four-hour food or water deprivation also caused rats with striatal lesions to consume more food during the subsequent 24 h. Motor deficits were found in rats with lesions, insofar as their ability to handle the food pellets was greatly impaired. Finally, d-amphetamine and fenfluramine-induced anorexia was significantly enhanced in animals with lesions. The similarities and dissimilarities in the feeding and drinking behaviors between the rats with neostriatal lesions and those with lateral hypothalamic and nigrostriatal lesions are discussed. Biochemical and histological examinations confirmed the specificity of the KA-induced lesions in destroying only neuronal cell bodies although sparing axons and fiber bundles transversing or terminating in the striatum. Combined with previous results showing biochemical, histological, and psychological similarities between rats with KA-induced striatal lesions and humans with Huntington's disease, the present results further strengthen the parallels between this animal model and the human state for which decreases in body weight and regulatory deficits are also symptomatic.