GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.

Have any questions? Please email us at ecoliwiki@gmail.com


Jump to: navigation, search


You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki

See Help for Help on this wiki. See the documentation for how to use the table editor


Kobayashi, T, Tonai, S, Ishihara, Y, Koga, R, Okabe, S and Watanabe, T (2000) Abnormal functional and morphological regulation of the gastric mucosa in histamine H2 receptor-deficient mice. J. Clin. Invest. 105:1741-9


To clarify the physiological roles of histamine H2 receptor (H2R), we have generated histamine H2R-deficient mice by gene targeting. Homozygous mutant mice were viable and fertile without apparent abnormalities and, unexpectedly, showed normal basal gastric pH. However, the H2R-deficient mice exhibited a marked hypertrophy with enlarged folds in gastric mucosa and an elevated serum gastrin level. Immunohistochemical analysis revealed increased numbers of parietal and enterochromaffin-like (ECL) cells. Despite this hypertrophy, parietal cells in mutant mice were significantly smaller than in wild-type mice and contained enlarged secretory canaliculi with a lower density of microvilli and few typical tubulovesicles in the narrow cytoplasm. Induction of gastric acid secretion by histamine or gastrin was completely abolished in the mutant mice, but carbachol still induced acid secretion. The present study clearly demonstrates that H2R-mediated signal(s) are required for cellular homeostasis of the gastric mucosa and normally formed secretory membranes in parietal cells. Moreover, impaired acid secretion due to the absence of H2R could be overcome by the signals from cholinergic receptors.


PubMed PMC378512 Online version:10.1172/JCI9441


Animals; DNA/analysis; Fertility; Gastric Acid/physiology; Gastric Mucosa/pathology; Gastric Mucosa/physiology; Gastric Mucosa/physiopathology; Homozygote; Hypertrophy; Mice; Mice, Knockout; Organ Size; Receptors, Histamine H2/deficiency; Receptors, Histamine H2/genetics; Receptors, Histamine H2/physiology; Restriction Mapping; Reverse Transcriptase Polymerase Chain Reaction