THE ROLE OF ECL CELLS IN SIGNALING WITHIN THE GASTRIC MUCOSA
Research field:Other
Authors:Håkanson R, Lindström E, Norlén P
Address of presenting
author:		Professor Rolf Håkanson
Institute of Physiological Sciences
Department of Pharmacology
Sölvegatan 10
S-223 62 Lund
Sweden
E-mail:Rolf.Hakanson@farm.lu.se
Phone:+46 46 2227585
Fax:+46 46 2224429
Text of abstract Introduction
ECL cells are peptide hormone-producing endocrine/paracrine cells occurring in the vertebrate oxyntic mucosa (Håkanson et al. 1994). In addition, the ECL cells produce histamine which mediates the stimulatory effect of gastrin on the acid-producing parietal cells. The gastrin-ECL cell pathway has been explored extensively both in vivo (gastric submucosal microdialysis) and in vitro (isolated ECL cells in primary culture). By comparison, the nervous control of the ECL cells is less well understood. The vagus and the sympathetic nervous system control enteric neurons in the myenteric/submucosal ganglia, and both parietal cells and ECL cells receive innervation from such neurons. Studies of isolated ECL cells in primary culture have revealed a strong stimulatory effect of PACAP and a moderate stimulatory effect of VIP and adrenaline (but not acetylcholine) and an inhibitory effect of somatostatin and galanin (Lindström et al. 1997). In addition, prostaglandin E2 suppressed ECL-cell activity.

Methods
The physiological control of ECL-cell activity in situ was studied by gastric submucosal microdialysis in conscious rats (Kitano et al. 2000). Histamine mobilization was stimulated by food intake or intravenous gastrin. Subsequently, numerous neurotransmitter candidates and several prostaglandins were applied locally by perfusion via the microdialysis probe.

Results
The stimulatory effects of gastrin infusion or food intake were virtually abolished by gastrin receptor blockade suggesting that gastrin is the major stimulus of food-evoked ECL-cell histamine mobilization. A number of candidate neurotransmitters, including PACAP, VIP and noradrenaline, were also effective stimulators of ECL-cell secretion. Acetylcholine was without effect. Somatostatin and prostaglandin E2 were powerful inhibitors of ECL-cell secretion. In addition, the neuropeptide galanin was found to be quite effective in inhibiting gastrin-stimulated histamine release.

Conclusions
Although the gastrin-ECL cell axis is a major pathway for controlling acid secretion in the rat stomach, neuromodulatory inputs to ECL cells and to parietal cells directly play an important role.

References
Håkanson, R., Chen, D. & Sundler, F. 1994 In: L.R. Johnson (ed.) Physiology of the Gastrointestinal Tract, pp 1171-1184. Raven Press, New York.
Lindström, E., Björkqvist, M., Boketoft, Å. , Chen, D., Zhao, C.-M., Kimura, K. & Håkanson, R. 1997. Regul Pept 71, 73-86
Kitano, M., Norlén, P. & Håkanson, R. 2000. Regul Pept 86, 113-123

Keywords:Acid secretion, gastrin, ECL cells, vagus, neuropeptides

Created 20000-05-11