Gastric ulceration and expression of prolactin receptor in the brain in Hatano high- and low-avoidance rats

Recently, prolactin was shown to inhibit the development of stress-induced ulcers. However, the mechanism for suppression of gastric ulcers by prolactin has not been clarified. Hatano high-avoidance (HAA) and low-avoidance (LAA) strains of rats were originally selected and bred from Sprague-Dawley rats based on shuttle-box tasks. The present study focused on the relationships among gastric ulceration and endocrine response with special reference to prolactin secretion and restraint stress in water of HAA and LAA rats. The restraint stress induced an elevation of plasma concentrations of ACTH, corticosterone, and prolactin. Peak levels of plasma ACTH during stressful condition were significantly higher in HAA rats than in LAA rats, while peak levels of prolactin were significantly lower in HAA rats than in LAA rats. The gastric erosion index was significantly higher in HAA rats than in LAA rats 7 h after restraint stress in water. The numbers of prolactin-receptor-positive cells determined by immunohistochemistry in the paraventricular nucleus was significantly increased in LAA rats than in HAA rats 7 h after restraint stress in water. These results indicate that HAA rats were more sensitive than LAA rats to restraint stress in water. The strain differences in gastric ulceration under stress may be involved in peripheral prolactin secretion and central prolactin receptor expression. The expression of prolactin receptor in the paraventricular nucleus may be important in suppressing gastric ulceration.