GLUCOCORTICOID REGULATION OF ANGIOTENSINOGEN GENE-EXPRESSION IN DISCRETE AREAS OF THE MALE-RAT BRAIN - AN IN-SITU HYBRIDIZATION STUDY

Citation
B. Bunnemann et al., GLUCOCORTICOID REGULATION OF ANGIOTENSINOGEN GENE-EXPRESSION IN DISCRETE AREAS OF THE MALE-RAT BRAIN - AN IN-SITU HYBRIDIZATION STUDY, Neuroendocrinology, 57(5), 1993, pp. 856-862
Citations number
35
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00283835
Volume
57
Issue
5
Year of publication
1993
Pages
856 - 862
Database
ISI
SICI code
0028-3835(1993)57:5<856:GROAGI>2.0.ZU;2-I
Abstract
The regulation of angiotensinogen gene expression by glucocorticoids h as been described in several studies. Kalinyak and Perlman reported on a 60% increase of angiotensinogen expression in the rat brain after d examethasone treatment with a single, high-dose injection. The purpose of the present study was to investigate whether a general upregulatio n of angiotensinogen expression or a region-specific upregulation unde rlies these findings. By using in situ hybridization and computer-assi sted microdensitometry we evaluated the regional changes in angiotensi nogen expression following dexamethasone treatment. Angiotensinogen ex pression was strongly stimulated in several areas (medial septum and l ocus ceruleus), while only moderately in others (hypothalamus, medulla ). An interesting finding is the difference in glucocorticoid receptor regulation among the circumventricular organs. The subfornical organ displayed no changes in angiotensinogen-mRNA, whereas the area postrem a showed an increase. Furthermore, the angiotensinogen expression in t he median eminence decreased substantially. The nature of these effect s will form the subject of further investigations. In conclusion we de monstrated an overall increase but certain heterogeneities in angioten sinogen expression after dexamethasone treatment, a pattern which sugg ests different degrees of glucocorticoid receptor regulation of the an giotensinogen gene in certain areas of the brain, probably mainly depe ndent on the degree of glial glucocorticoid receptor presence.