Cellular immunity is not compromised by high serum corticosterone
concentrations in prairie voles (microtus ochrogaster).
Klein, Sabra L., Susan E. Taymans, A. Courtney Devries, and Randy J.
Nelson.
Department of Psychology, Behavioral Neuroendocrinology Group,
Population Dynamics, The Johns Hopkins University, Baltimore, MD
21218-2686 USA; Developmental, Endocrinology Branch, NICHD, National
Institutes of Health, Bethesda, MD 20892 USA
APStracts 3:0265R, 1996.
Glucocorticoids compromise immune function in glucocorticoid-sensitive
species (e.g., mice), but these immunosuppressive effects may be
reduced in glucocorticoid-resistant species. Prairie voles (Microtus
ochrogaster) have been characterized as glucocorticoid-resistant to
their high circulating levels of corticosterone. Because
glucocorticoid-sensitive species display suppressed lymphocyte
proliferation in response to elevated blood glucocorticoid levels,
proliferative values were hypothesized to be reduced in house mice
(Mus musculus) as compared to prairie voles. Prairie voles exhibited
significantly higher splenocyte proliferative responses to the T-cell
mitogen, Concanavalin A, despite having higher basal total and free
serum corticosterone levels than mice. Neither total nor free serum
corticosterone correlated with proliferative responses from either
species. These data provide further evidence for glucocorticoid
-resistance in prairie voles, and suggest that the interactions
between the hypothalamic-pituitary-adrenal (HPA) axis and the immune
system in prairie voles may differ from those in mice or other
glucocorticoid-sensitive species. Therefore, prairie voles may serve
as a valuable animal model for the syndrome of glucocorticoid
-resistance in humans, and the role of glucocorticoids in conditions
characterized by a hyperactive immune system.
Received 27 March 1996; accepted in final form 17 June 1996.
APS Manuscript Number R185-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996