Based on an invited presentation in the Symposium on Food intake-related control of gut function at the joint meeting of the Scandinavian and German Physiological Societies, Copenhagen, March, 2010.
Plasticity in vagal afferent neurones during feeding and fasting: mechanisms and significance*
Article first published online: 1 FEB 2011
© 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society
Volume 201, Issue 3, pages 313–321, March 2011
How to Cite
Dockray, G. J. and Burdyga, G. (2011), Plasticity in vagal afferent neurones during feeding and fasting: mechanisms and significance. Acta Physiologica, 201: 313–321. doi: 10.1111/j.1748-1716.2010.02219.x
- Issue published online: 1 FEB 2011
- Article first published online: 1 FEB 2011
- Accepted manuscript online: 10 NOV 2010 01:57AM EST
- Received 31 August 2010, revision requested 17 October 2010, revision received 28 October 2010, accepted 2 November 2010
- CB1 receptors;
- cocaine and amphetamine regulated transcript;
- melanin concentrating hormone;
- Y2 receptors
The ingestion of food activates mechanisms leading to inhibition of food intake and gastric emptying mediated by the release of regulatory peptides, for example cholecystokinin (CCK), and lipid amides, e.g. oleylethanolamide from the gut. In addition, there are both peptides (e.g. ghrelin) and lipid amides (e.g. anandamide) that appear to signal the absence of food in the gut and that are associated with the stimulation of food intake. Vagal afferent neurones are a common target for both types of signal. Remarkably, the neurochemical phenotype of these neurones itself depends on nutritional status. CCK acting at CCK1 receptors on vagal afferent neurones stimulates expression in these neurones of Y2-receptors and the neuropeptide CART, both of which are associated with the inhibition of food intake. Conversely, in fasted rats when plasma CCK is low, these neurones express cannabinoid (CB)-1 and melanin concentrating hormone (MCH)-1 receptors, and MCH, and this is inhibited by exogenous CCK or endogenous CCK released by refeeding. The stimulation of CART expression by CCK is mediated by the activation of CREB and EGR1; ghrelin inhibits the action of CCK by promoting nuclear exclusion of CREB and leptin potentiates the action of CCK by the stimulation of EGR1 expression. Vagal afferent neurones therefore constitute a level of integration outside the CNS for nutrient-derived signals that control energy intake and that are capable of encoding recent nutrient ingestion.