Abstract 11beta-Hydroxysteroid dehydrogenase (11beta-OHSD) metabolizes corticosterone to inactive 11-dehydrocorticosterone and thus protects non-specific mineralocorticoid receptors from exposure to corticosterone in the kidney in vivo. Clearly, 11beta-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 11beta-OHSD bioactivity with similar co-substrate requirements and inhibition kinetics to the renal enzyme. 11beta-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 11beta-OHSD in cerebellum and suggest that it may regulate the access of corticosterone to glucocorticoid receptors in addition to mineralocorticoid receptors.
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Moisan et al. (1990) studied this question.
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