Attenuation of Hippocampal 11beta-Hydroxysteroid Dehydrogenase Type 1 by Chronic Psychosocial Stress in the Tree Shrew

K. Jamieson, E. Fuchs, [No Value] Flugge, M J Seckl, Pauline Jamieson

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) catalyses the interconversion of active cortisol and corticosterone with inert cortisone and 11-dehydrocorticosterone, thus regulating glucocorticoid access to intracellular receptors. In rats, chronic glucocorticoid excess or stress increases 11beta-HSD-1 in the hippocampus, producing suggestions that it may attenuate the deleterious effects of chronic glucocorticoid excess. However, 11beta-HSD-1 predominantly catalyses 11beta-reduction in the intact liver and hippocampal cells, thus regenerating active glucocorticoids from inert substrate. We studied 11beta-HSD activity in the tissues of male tree shrews following 28 days of sustained psychosocial stress or exogenous administration of cortisol. In the hippocampus, chronic psychosocial stress attenuated 11-HSD-1 activity (69 +/- 9% of control), whereas cortisol alone had no effect. In the liver, both chronic stress and cortisol administration decreased 11beta-HSD-1 activity (47 +/- 11% and 49 +/- 4% fall, resp.). Attenuation of 11beta-HSD-1 within tissues may reflect a homeostatic mechanism designed to minimise the adverse effects of prolonged stress and/or glucocorticoid excess.
Original languageEnglish
Pages (from-to)123-132
Number of pages10
JournalStress: The International Journal on the Biology of Stress
Volume2
Issue number2
Publication statusPublished - 1997

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