Functional analyses of gastric mucosa using mice deficient in both histamine H_2 receptor and CCK_B/gastrin receptor

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To decipher the roles of gastrin and histamine H_2 receptors in gastric mucosa, mice deficient in both were generated and analyzed. Double-null mice exhibited atrophy of gastric mucosae, marked hypergastrinemia and higher gastric pH than gastrin receptor-null mice, which was unresponsive even to carbachol. Comparison of gastric mucosae from 10-week-old wild type, H_2 receptor-null, gastrin receptor-null and double-null mice revealed unique roles of these receptors in gastric mucosa. While small parietal cells and increases in the number and mucin contents of mucous neck cells were secondary to impaired acid production, H_2 receptor was responsible for chief cell maturation. In double-null and gastrin receptor-null mice, despite gastric mucosal atrophy, surface mucous cells were significantly increased, in contrast to gastrin-null mice. Other gastrin-gene product than gastrin-17 may be responsible for the increase independently of the H_2 receptor. Thus, different GPCRs affect differentiation into different cells derived from common stem cells in gastric mucosa.