Abstract
11-beta-Hydroxysteroid dehydrogenase (11-beta-OHSD) metabolizes corticosterone to inactive 11-dehydrocorticosterone and thus protects non-specific mineralocorticoid receptors from exposure to corticosterone in the kidney in vivo. Clearly, 11-beta-OHSD might also regulate corticosterone access to glucocorticoid receptors. We have investigated cerebellum, a tissue with high glucocorticoid receptor, but very low mineralocorticoid receptor levels and have shown marked 11-beta-OHSD bioactivity with similar co-substrate requirements and inhibition kinetics to the renal enzyme. 11-beta-OHSD messenger ribonucleic acid was expressed in cerebellum and was localized in Purkinje and granule cells. This distribution was confirmed immunohistochemically. Thus, we provide evidence for 11-beta-OHSD in cerebellum and suggest that it may regulate the access of corticosterone to glucocorticoid receptors in addition to mineralocorticoid receptors.
Original language | English |
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Pages (from-to) | 853-858 |
Number of pages | 6 |
Journal | Journal of Neuroendocrinology |
Volume | 2 |
Issue number | 6 |
Publication status | Published - 1990 |