Effects of Experimentally Elevated Testosterone on Plasma Corticosteroid Binding Globulin in Dark-Eyed Juncos (Junco hyemalis)

Document Type

Article

Publication Date

10-1-1997

Publication Title

General and Comparative Endocrinology

DOI

10.1006/gcen.1997.6956

ISSN

0016-6480

Abstract

An earlier study of free-living male dark-eyed juncos found an increase in plasma corticosterone (B) in response to experimental elevation of plasma testosterone (T) (E. D. Ketterson et al., 1991, Horm. Behav. 25, 489-503). To investigate whether the increase was caused by enhanced secretion of corticosterone or by a slower clearance rate, or both, we exposed 52 captive yearling male dark-eyed juncos (Junco hyemalis) to day lengths corresponding to those of spring and implanted them with one or two testosterone-filled or sham implants (10 T-I, 22 T-II, and 20 C-males). We then examined the effect of experimentally elevated testosterone on plasma corticosterone and on corticosteroid-binding globulin (CBG), as measured by the ability of steroid-stripped plasma to bind labeled corticosterone. Plasma samples were taken five times, 2 weeks before experimental prolongation of day length and approximately every 3 weeks thereafter. Treatment with testosterone increased both plasma testosterone and plasma corticosterone two to three times above control levels, and the degree of elevation was dose-dependent. Only when all treatment groups were pooled, however, were plasma testosterone and corticosterone significantly correlated. The relationship between plasma corticosterone and time required to bleed the birds was similar for all three treatment groups, suggesting that there was no effect of treatment on the stress response. Testosterone significantly increased the capacity of the plasma to bind corticosterone, presumably because it contained more CBG, when compared to the plasma of controls. However, treatment with testosterone did not affect the affinity of the plasma for corticosterone. It seems likely that exogenous testosterone elevated corticosterone by slowing the corticosterone clearance rate via an increase in CBG. It is not clear what the net effect of chronic elevation of testosterone would be on the availability of corticosterone to target tissues.

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