The central mechanism that mediates litorin-induced satiety is poorly understood, and has not been studied in a non-mammalian species. Therefore, the aim of this study was to determine if litorin-induced satiety in an alternative vertebrate model, the chick, and to elucidate some of the central mechanisms that are associated with this response. In Experiment 1, chicks responded to intracerebroventricular (ICV) injection of litorin with reduced food intake at all doses tested (0.1, 1.0, and 10 nmol), while concurrently, an anti-dipsogenic effect was observed in the two higher doses tested. Whole blood glucose concentrations were not affected. In Experiment 2, chicks that were food-withheld did not reduce their water intake after ICV litorin injection. To determine if litorin affected behaviors unrelated to ingestion, a comprehensive behavior analysis was conducted as Experiment 3. Of the behaviors observed, only the number of feeding pecks was reduced. Other behaviors such as movement, defecation, escape, posture, or deep rest were not affected. Lastly, in Experiment 4, litorin-treated chicks had an increased number of c-Fos immunoreactive cells in the magnocellular division of the paraventricular nucleus. The arcuate nucleus, dorsomedial nucleus, lateral hypothalamus, parvicellular division of the paraventricular nucleus, suprachiasmatic nucleus, periventricular nucleus and the ventromedial hypothalamus were not affected. Therefore, we conclude that ICV litorin causes anorexigenic effects in chicks associated with changes in hypothalamic chemistry that appear to be behavior specific.