In a strain of inbred cotton rats, 25-50% of females develop spontaneous gastric hypochlorhydria and hypergastrinemia. Hypergastrinemic animals develop ECL cell derived gastric carcinomas located in the oxyntic mucosa, thus being an interesting animal model for studying the role of gastrin in gastric carcinogenesis. The response to gastric hypoacidity in cotton rats as regards the level of hypergastrinemia is far more pronounced than in the more commonly used laboratory rat. It is unknown whether the pronounced hypergastrinemic response in cotton rats is due to a greater population of G cells or a greater capacity of hormone synthesis in each G cell. The aim of the study was therefore to examine G cell population and ultrastructure in normogastrinemic and hypergastrinemic cotton rats by the use of immunhistochemical methods applied on both light- and electron-microscopy. Five hypergastrinemic vs. five normogastrinemic cotton rats were compared. Cotton rats with gastric hypochlorhydria have a 55-fold increase in serum gastrin levels and a 6-fold increase in G cell number, but this is not accompanied by significant changes in G cell ultrastructure. The lack of ultrastructural changes in these activated G cells indicates that previously reported changes in chronic stimulated G cells are just one of several ways G cells are activated.
