Effect of chronic intermittent immobilization stress on hypophyso-gonadal function of rats

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Abstract
The neuroendocrine mechanisms involved in chronic stress-induced testosterone (T) suppression were evaluated in adult male rats. In intact animals, restraint applied 6 h daily for 6 days increased plasma corticosterone, decreased significantly T and Prl [prolactin], and, to a lesser degree, LH [lutropin] levels. In adrenalectomized (adr-x) rats exposed to the same stress regimen, plasma LH and T values were reduced, whereas Prl concentrations were significantly elevated as compared with intact stressed rats. Adrenalectomy alone did not modify basal levels of these hormones. In intact rats, chronic stress did not alter the amount of [125I]iodo-hCG [human chorionic gonadotropin] specifically bound to crude testis membrane preparation, or the testicular responsiveness to hCG as measured by T levels 2 h after hCG injection (500 IU). In adr-x groups a significant decrease in binding capacity of [125I]iodo-hCG and no alteration in hCG responsiveness were observed. Apparently plasma T suppression induced by chronic restraint is not initially mediated by a direct action at the testis level as judged by the normal testicular hCG binding capacity and responsiveness to hCG; the sustained endogenous release of glucocorticoid associated with chronic restraint exposure does not play an important role in the decrease of LH and T secretion but could participate in the Prl drop induced by long-term exposure to stressors and the decrease in LH secretion may be partly responsible for the T suppression, whereas follitropin (on the basis of previous observations) and Prl do not seem to exert a significant role.