Corticotropin-releasing factor (CRF) has been hypothesized to modulate consummatory behavior through the Type 2 CRF (CRF 2 ) receptor. However, behavioral functions subserved by the CRF 2 receptor remain poorly understood. Recently, human urocortin II (hUcn II), a selective CRF 2 receptor agonist, was identified. To study the effects of this neuropeptide on ingestive behavior, we examined the effects of centrally infused hUcn II (i.c.v. 0, 0.01, 0.1, 1.0, 10.0 g) on the microstructure of nosepoke responding for food and water in nondeprived, male rats. Malaise-inducing properties of the peptide were monitored using conditioned taste aversion (CTA) testing. To identify potential sites of action, central induction of Fos protein expression was examined. hUcn II dose dependently reduced the quantity and duration of responding for food and water at doses lower (0.01-1.0 g) than that forming a CTA (10 g). Effects were most evident during hours 4 to 6 of the dark cycle. Meal pattern analysis showed that hUcn II potently (0.1 g) increased the satiating value of food. Rats ate and drank smaller and shorter meals without changing meal frequency. Rats also ate more slowly. hUcn II induced Fos in regions involved in visceral sensory processing and autonomic/neuroendocrine regulation and resembling those activated by appetite suppressants. hUcn II is a promising neuropeptide for investigating the role of the CRF 2 receptor in ingestive behavior.Corticotropin-releasing factor (CRF) is hypothesized to mediate behavioral, autonomic, endocrine, and immunological responses to stress (Koob and Heinrichs, 1999). Intracerebroventricular (i.c.v.) administration of CRF in rats mimics several behavioral effects of stress, including motor activation, anxiety-like behavior, anorexia, reduced sexual behavior, and altered cognitive performance (Koob et al., 1994). Two genes encoding separate families of G-protein coupled CRF receptors, each having distinct distributions and functional and pharmacological properties (Perrin and Vale, 1999), have been identified (CRF 1 and CRF 2 ). Whereas molecular and receptor antagonist studies point to activating and anxiogenic-like roles of the CRF 1 receptor (Koob and Heinrichs, 1999), behavioral functions mediated by the CRF 2 receptor have remained obscure.