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11Beta‐Hydroxysteroid Dehydrogenase Messenger Ribonucleic Acid Expression, Bioactivity and Immunoreactivity in Rat Cerebellum
Author(s) -
Moisan MariePierre,
Seckl Jonathan R.,
Brett Lawrence P.,
Monder Carl,
Agarwal Anil K.,
White Perrin C.,
Edwards Christopher R. W.
Publication year - 1990
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1990.tb00651.x
Subject(s) - medicine , endocrinology , corticosterone , mineralocorticoid , mineralocorticoid receptor , glucocorticoid , glucocorticoid receptor , receptor , biology , cerebellum , chemistry , aldosterone , hormone
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.