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.
|Number of pages||6|
|Journal||Journal of Neuroendocrinology|
|Publication status||Published - 1990|