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

作者信息

Ray A, Henke P G, Sullivan R M

机构信息

Department of Psychology, St. Francis Xavier University, Antigonish, N.S., Canada.

出版信息

Neurosci Lett. 1990 Mar 14;110(3):331-6. doi: 10.1016/0304-3940(90)90869-b.

DOI:10.1016/0304-3940(90)90869-b
PMID:2325904
Abstract

Microinjections of noradrenaline (NA, 0.3, 3.0 and 30.0 micrograms) into the central amygdalar nucleus (CEA) produced dose-related attenuations of cold restraint (3 h at 4 degrees C) induced gastric ulcer formation in rats. On the other hand, stress ulcer aggravating effects were seen with beta-adrenoceptor antagonist, propranolol (10 micrograms) but not with the alpha-adrenoceptor antagonist, prazosin (1 and 10 micrograms). Moderate enhancements of gastric stress lesions were also seen with the NA release inhibitor clonidine (1 microgram) and the neurotoxin DSP-4 (25 micrograms). 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 beta-adrenoceptor-mediated NAergic mechanisms at the level of the CEA are important for the maintenance of gastric mucosal integrity during immobilization stress.

摘要

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