11BETA-HYDROXYSTEROID DEHYDROGENASE MESSENGER-RIBONUCLEIC-ACID EXPRESSION, BIOACTIVITY AND IMMUNOREACTIVITY IN RAT CEREBELLUM

M P  MOISAN; J R  SECKL; L P  BRETT; C  MONDER; A K  AGARWAL; P C  WHITE; C R W  EDWARDS

11BETA-HYDROXYSTEROID DEHYDROGENASE MESSENGER-RIBONUCLEIC-ACID EXPRESSION, BIOACTIVITY AND IMMUNOREACTIVITY IN RAT CEREBELLUM

M P MOISAN, J R SECKL, L P BRETT, C MONDER, A K AGARWAL, P C WHITE, C R W EDWARDS

Deanery of Clinical Sciences

Research output: Contribution to journal › Article › peer-review

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
Pages (from-to)	853-858
Number of pages	6
Journal	Journal of Neuroendocrinology
Volume	2
Issue number	6
Publication status	Published - 1990

Cite this

@article{496ac6c2fac646c99917c5b44a2d187b,

title = "11BETA-HYDROXYSTEROID DEHYDROGENASE MESSENGER-RIBONUCLEIC-ACID EXPRESSION, BIOACTIVITY AND IMMUNOREACTIVITY IN RAT CEREBELLUM",

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.",

author = "MOISAN, {M P} and SECKL, {J R} and BRETT, {L P} and C MONDER and AGARWAL, {A K} and WHITE, {P C} and EDWARDS, {C R W}",

year = "1990",

language = "English",

volume = "2",

pages = "853--858",

journal = "Journal of Neuroendocrinology",

issn = "0953-8194",

publisher = "Blackwell Publishing",

number = "6",

}

TY - JOUR

T1 - 11BETA-HYDROXYSTEROID DEHYDROGENASE MESSENGER-RIBONUCLEIC-ACID EXPRESSION, BIOACTIVITY AND IMMUNOREACTIVITY IN RAT CEREBELLUM

AU - MOISAN, M P

AU - SECKL, J R

AU - BRETT, L P

AU - MONDER, C

AU - AGARWAL, A K

AU - WHITE, P C

AU - EDWARDS, C R W

PY - 1990

Y1 - 1990

N2 - 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.

AB - 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.

M3 - Article

VL - 2

SP - 853

EP - 858

JO - Journal of Neuroendocrinology

JF - Journal of Neuroendocrinology

SN - 0953-8194

IS - 6

ER -