Brain regions where cholecystokinin exerts its effect on satiety

Abstract

The neuropeptide cholecystokinin (CCK), which is localized within the hypothalamus in integrative centers of feeding regulation, can suppress feeding behavior when exogenously applied into the lateral hypothalamus. Moreover, the endogenous peptide can be released from the same brain locus by stimuli that physiologically are associated with satiety (i.e., gastric meal loads). This endogenously released CCK contributes to the inhibition of feeding behavior during meal intake. These data strongly suggest that hypothalamic CCK may play a physiological role in the termination of feeding behavior. The presence of additional sites sensitive to CCK in extrahypothalamic regions (e.g., medial pons and lateral medulla) argue that the CCK receptor systems may functionally (1) have several links in a linear chain or (2) exist as several parallel systems. The relevance of these extrahypothalamic loci for feeding regulation will require further studies which need to be directed towards the physiological role of the endogenously released CCK in these particular areas, by use of selective CCK antagonists.