Nibbling at CRF receptor control of feeding and gastrocolonic motility

Inadequate pharmacological tools, until recently, hindered the understanding of the roles of corticotropin-releasing factor (CRF) receptor subtypes in appetite regulation and gastrocolonic motor function. Now, novel ligands that are selective for CRF 1 or CRF 2 receptors are helping to uncover the s...

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Bibliographic Details
Published in:Trends in pharmacological sciences (Regular ed.) 2003-08, Vol.24 (8), p.421-427
Main Authors: Zorrilla, Eric P, Taché, Yvette, Koob, George F
Format: Article
Language:English
Subjects:
Animals
Brain - metabolism
Brain - physiology
Colon - physiology
Corticotropin-Releasing Hormone - metabolism
Eating - physiology
Gastrointestinal Motility - physiology
Humans
Intestines - metabolism
Intestines - physiology
Ligands
Receptors, Corticotropin-Releasing Hormone - agonists
Receptors, Corticotropin-Releasing Hormone - metabolism
Receptors, Corticotropin-Releasing Hormone - physiology
Satiation - physiology
Stress, Physiological - metabolism
Stress, Physiological - physiopathology
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Summary:Inadequate pharmacological tools, until recently, hindered the understanding of the roles of corticotropin-releasing factor (CRF) receptor subtypes in appetite regulation and gastrocolonic motor function. Now, novel ligands that are selective for CRF 1 or CRF 2 receptors are helping to uncover the specific functions of CRF receptor subtypes. Central or peripheral CRF 2 receptor activation suppresses feeding independently of CRF 1 receptors. In the rat, central administration of CRF 2 receptor agonists promotes satiation without eliciting the malaise, behavioral arousal or anxiogenesis associated with CRF 1 receptor agonists. Conversely, central administration of CRF 1 receptor agonists elicits short-onset anorexia independently of CRF 2 receptor activation. With respect to gastrointestinal motor function, stress inhibits gastric motility through CRF 2 receptor-dependent central autonomic and peripheral myenteric systems. By contrast, stress stimulates colonic motility via CRF 1 receptor-dependent sacral parasympathetic and colonic myenteric mechanisms. These findings have important physiological implications and suggest targeted approaches for the pharmacotherapy of obesity and stress-related functional gastrointestinal and eating disorders.
ISSN:0165-6147
1873-3735
DOI:10.1016/S0165-6147(03)00177-9