CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

1 University of Groningen, Haren, The Netherlands; and 2 Programs in Neuroscience and Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington Submitted 30 November 2004 ; accepted in final form 10 May 2005 Capsaicin treatment d...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2005-09, Vol.289 (3), p.R695-R703
Main Authors: van de Wall, E. H. E. M, Duffy, P, Ritter, R. C
Format: Article
Language:English
Subjects:
Animals
Area Postrema - metabolism
Capsaicin - pharmacology
Catheterization
Cholecystokinin - pharmacology
Drug Resistance
Male
Neurons, Afferent - drug effects
Neurons, Afferent - physiology
Proto-Oncogene Proteins c-fos - metabolism
Rats
Rats, Sprague-Dawley
Rhombencephalon - drug effects
Rhombencephalon - metabolism
Solitary Nucleus - metabolism
Stomach - drug effects
Stomach - physiology
Tissue Distribution
Vagus Nerve - drug effects
Vagus Nerve - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:1 University of Groningen, Haren, The Netherlands; and 2 Programs in Neuroscience and Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington Submitted 30 November 2004 ; accepted in final form 10 May 2005 Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension. Fos; dorsal vagal complex; C fibers; A fibers Address for reprint requests and other correspondence: E. H. E. M. van de Wall, Univ. of Groningen, Dept. of Neuroendocrinology, PO Box 14, 9750 AA Haren, The Netherlands
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00809.2004