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Departments of Physiology and Medicine, University of California, Los Angeles, and Department of Veterans Affairs Greater Los Angeles Health System, West Los Angeles Healthcare Center, Los Angeles, California 90073
The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in rabbit gastric glands using confocal microscopy. Intracellular calcium concentration ([Ca2+]i) changes were used to monitor cellular responses. Histamine and carbachol increased [Ca2+]i in parietal cells. Gastrin (1 nM) increased [Ca2+]i in ECL cells and adjacent parietal cells. Only the increase of [Ca2+]i in parietal cells was inhibited by H2 receptor antagonists (H2RA). Gastrin (10 nM) evoked an H2RA-insensitive [Ca2+]i increase in parietal cells. Carbachol produced large H2RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated [Ca2+]i in ECL cells and adjacent parietal cells. H2RAs abolished the PACAP-stimulated [Ca2+]i increase in adjacent parietal cells. Somatostatin did not inhibit the increase of [Ca2+]i in parietal cells stimulated with histamine, high gastrin concentrations, or carbachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B receptors coupled to calcium signaling but insensitive to somatostatin, whereas rabbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors sensitive to somatostatin.
gastrin; histamine; pituitary adenylate cyclase-activating peptide; somatostatin; enterochromaffin-like cell
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