The marked functional similarities between pharmacological effects of bombesin and of corticotropin-releasing factor (CRF), prompted the formulation and testing of our working hypothesis that BN may elicit its biological effects through the release of CRF. Central pretreatment with CRF receptor antagonists, α-helical CRF-(9-41)(α-CRF-(9-41)) or [D-Phe12, C(α)MeLeu37]CRF-(12-41) (CαMeCRF), blocked the effects of centrally administered bombesin on food intake and related behaviors and partially attenuated the satiety effects of systemically administered bombesin. We also attempted to characterize the specificity of this interaction through the combined use of bombesin with the oxytocin antagonist, Ed(CH2)5, Tyr(OMe)2, Orn8]vasotocin (vasotocin). Central pretreatment with vasotocin failed to alter bombesin-induced behaviors, suggesting the absence of a pharmacological interaction between these two peptidergic systems. Finally, the CRF antagonist failed to reverse the oxytocin-induced suppression of food intake, indicating that CRF does not have a direct role in the mediation and/or modulation of the effects of oxytocin on food intake. Thus, the present experiments support the contention that bombesin partly mediates its feeding-suppressant effects through interactions with CRF. The specificity of this interaction is supported by the lack of interaction between bombesin and/or CRF with oxytocin.
- Central nervous system
- GRP(Gastrin-releasing peptide)