Systemic cholecystokinin amplifies vago-vagal reflex responses recorded in vagal motor neurones
- 1Laboratory of Autonomic Neurosciences, Pennington Biomedical Research Centre, Louisiana State University System, Baton Rouge, LA 70808, USA
- G. E. Hermann: Pennington Biomedical Research Centre, 6400 Perkins Rd, Baton Rouge, LA 70808, USA. Email: gerlinda.hermann{at}pbrc.edu
Non-technical summary
Cholecystokinin (CCK) is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein; it also functions to suppress feeding. CCK is also recognized as a neurotransmitter within the central nervous system (CNS). As such, there are receptors for CCK both in the periphery as well as within the CNS. Thus, it is not certain where the principal site of action is for CCK to affect gastric reflexes and feeding behaviour. We show that picomole amounts of systemic CCK are sufficient to modulate gastric reflexes and that these effects are probably mediated via peripheral vagal afferents in the proximal gut. Knowledge of how and where this peptide hormone acts increases our understanding of the regulation of feeding behaviour.
Abstract
Cholecystokinin (CCK) is a potent regulator of visceral functions as a consequence of its actions on vago-vagal reflex circuit elements. This paper addresses three current controversies regarding the role of CCK to control gastric function via vago-vagal reflexes. Specifically: (a) whether CNS vs. peripheral (vagal afferent) receptors are dominant, (b) whether the long (58) vs. short (8) isoform is more potent and (c) whether nutritional status impacts the gain or even the direction of vago-vagal reflexes. Our in vivo recordings of physiologically identified gastric vagal motor neurones (gastric-DMN) involved in the gastric accommodation reflex (GAR) show unequivocally that: (a) receptors in the coeliac–portal circulation are more sensitive in amplifying gastric vagal reflexes; (b) in the periphery, CCK8 is more potent than CCK58; and (c) the nutritional status has a marginal effect on gastric reflex control. While the GAR reflex is more sensitive in the fasted rat, CCK amplifies this sensitivity. Thus, our results are in stark contrast to recent reports which have suggested that vago-vagal reflexes are inverted by the metabolic status of the animal and that this inversion could be mediated by CCK within the CNS.
- © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society
