Lactation in mammals is characterized by a marked hyperphagia and significantly elevated levels of prolactin (PRL). Several recent experiments in our laboratory have provided evidence for a causal relationship between PRL and hyperphagia. The present series of studies revealed that PRL injected intracerebroventricularly (i.c.v.) twice daily for ten days to free feeding virgin female rats produced a dose-dependent increase in food intake without disrupting vaginal cyclicity, that the hyperphagic effect of centrally administered PRL was not dependent on the presence of ovarian hormones, that it did not selectively potentiate feeding during the light or dark phase of the daily light cycle and that the latency of the feeding response to i.c.v. PRL administration was shorter in food restricted animals. Taken together, these results support the idea that PRL acts centrally to potentiate food intake.