Abstract
11β‐Hydroxysteroid dehydrogenase (11β‐OHSD) metabolizes corticosterone to inactive 11‐dehydrocorticosterone and thus protects non‐specific mineralocorticoid receptors from exposure to corticosterone in the kidney in vivo. Clearly, 11β‐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 11β‐OHSD bioactivity with similar co‐substrate requirements and inhibition kinetics to the renal enzyme. 11β‐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 11β‐OHSD in cerebellum and suggest that it may regulate the access of corticosterone to glucocorticoid receptors in addition to mineralocorticoid receptors.
Original language | English (US) |
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Pages (from-to) | 853-858 |
Number of pages | 6 |
Journal | Journal of Neuroendocrinology |
Volume | 2 |
Issue number | 6 |
DOIs | |
State | Published - Dec 1990 |
Keywords
- 11β‐hydroxysteroid dehydrogenase
- cerebellum
- corticosterone
- in situ hybridization
- steroid receptors
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology
- Endocrine and Autonomic Systems
- Cellular and Molecular Neuroscience