Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
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Experimental Manipulation of Corticosterone Does Not Influence the Clearance Rate of Plasma Testosterone in Birds.

In vertebrates, exposure to acute stressors stimulates the secretion of adrenal glucocorticoids such as corticosterone, and in some situations this hormone plays an important role in orchestrating the trade-off that exists between reproduction and self-maintenance. Stressful conditions often lead to a decrease in plasma levels of sex steroids such as testosterone in males, and it has been hypothesized that corticosterone contributes to this decrease. Generally supporting this proposition, glucocorticoids can inhibit the reproductive axis activity at multiple levels, including direct effects on testicular endocrine function. Here we tested for the first time the additional hypothesis that stress-induced glucocorticoids are associated with an increased clearance rate of circulating testosterone. To test this hypothesis, we performed two experiments comparing changes in plasma testosterone as a function of time (6-60 min) after a single injection of this hormone into captive male house finches (Haemorhous mexicanus) that either were intact (controls) or were pharmacologically adrenalectomized by administration of the glucocorticoid synthesis inhibitor mitotane. Control finches rapidly elevated their plasma corticosterone in response to handling, whereas mitotane treatment abolished this response by approximately 95%. Contrary to our prediction, we found no clear evidence that control birds eliminated exogenous testosterone from circulation at a different rate than pharmacologically adrenalectomized finches. These findings do not support the hypothesis that, during acute stress, elevated plasma glucocorticoids stimulate the clearance rate of testosterone. The rapid inhibitory effect of stress on plasma testosterone may rather result from direct actions of glucocorticoids on the gonadal production of the androgen or involve a glucocorticoid-independent mechanism.

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