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1 Department of Neuroendocrinology, University of Groningen, Haren, The Netherlands
* To whom correspondence should be addressed. E-mail: E.H.E.M.van.de.Wall{at}rug.nl.
Capsaicin-treatment destroys vagal afferent C-fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by cholecystokinin (CCK). However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Since 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 IP CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), while 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.
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