CRF-deficient mice respond like wild-type mice to hypophagic stimuli

Corticorropin-releasing factor (CRF) has been implicated in physiological p rocesses associated with stress, including changes in feeding behavior. Int racerebroventricular (ICV) administration of CRF and urocortin have been sh own to depress feeding, and antagonism of CRF receptors has been reported t o attenuate hypophagic responses to many treatments, suggesting that brain CRF may mediate these responses. We have now studied feeding behavior of mi ce lacking the CRF gene (CRFko), comparing them to wild-type (CRFwt) mice. Feeding was assessed in nondeprived mice by measuring the intake of sweeten ed milk in a 30-min period and the food pellet intake over 24 h. ICV admini stration of CRF or urocortin (1 mu g, but not lower doses) depressed milk a nd food pellet intake in normal mice. Physical restraint for 30 min, or adm inistration of mouse interleukin-lp (mIL-1 beta, 100 ng, IF), lipopolysacch aride (LPS, 1 mu g, IF), or the serotonergic agonist (d-fenfluramine, 4 mg/ kg, IF) reliably reduced milk intake. LPS also reduced food pellet intake. The responses to restraint, IL-1, LPS, and fenfluramine were indistinguisha ble between the CRFwt and CRFko mice. These results suggest that CRF is not essential for the reduction in sweetened milk intake that occurs following restraint, LPS, IL-1, or d-fenfluramine administration to mice. (C) 1999 E lsevier Science Inc.