Long-term corticosteroid treatment but not chronic stress affects 11β-hydroxysteroid dehydrogenase type I activity in rat brain and peripheral tissues

Peter H. Jellinck, Firdaus S. Dhabhar, Randall R. Sakai, Bruce S. McEwen

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Long-term treatment (21 days) of male rats with corticosterone in the drinking water caused a significant increase in the activity of the NADP-dependent form of 11β-hydroxysteroid dehydrogenase (11-HSD1) in the pituitary, thymus, and spleen, (marginally in the hippocampus, amygdala and lymph nodes), without having any effect in a number of other central and peripheral tissues. In contrast, repeated restraint stress, although increasing plasma corticosterone to the same level as that observed after its administration, failed to change the activity of this key regulatory enzyme, which allows aldosterone to exert its specific effects in the presence of a large excess of corticosterone. This resistance to elevation in 11-HSD activity was also observed in the thymuses of subordinate rats during social stratification in a visible burrow system. In both cases, the circulating levels of corticosterone were much higher in stressed rats than in control animals. Factors which might account for these differences in response are discussed and compared with the situation in intact cells where, unlike in tissue homogenates, the reduction of 11-dehydrocorticosterone to corticosterone (reductase activity) appears to predominate.

Original languageEnglish (US)
Pages (from-to)319-323
Number of pages5
JournalJournal of Steroid Biochemistry and Molecular Biology
Volume60
Issue number5-6
DOIs
StatePublished - Mar 1997
Externally publishedYes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Endocrinology
  • Clinical Biochemistry
  • Cell Biology

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