Noradrenergic mechanisms in the central amygdalar nucleus and gastric stress ulcer formation in rats

Abstract

Microinjections of noradrenaline (NA, 0.3, 3.0 and 30.0 μg) into the central amygdalar nucleus (CEA) produced dose-related attenuations of cold restraint (3 h at 4°C) induced gastric ulcer formation in rats. On the other hand, stress ulcer aggravating effects were seen with β-adrenoceptor antagonist, propranolol (10 μg) but not with the α-adrenoceptor antagonist, prazosin (1 and 10 μg). Moderate enhancements of gastric stress lesions were also seen with the NA release inhibitor clonidine (1 μg) and the neurotoxin DSP-4 (25 μg). Further, pretreatment of rats with intra-amygdalar (i.am.) propranolol but not prazosin, antagonized and reversed the gastric cytoprotective effects of NA. The results indicate that β-adrenoceptor-mediated NAergic mechanisms at the level of the CEA are important for the maintenance of gastric mucosal integrity during immobilization stress.