The neuroendocrine mechanisms involved in chronic stress-induced testosterone (T) suppression have been evaluated in adult male rats. In intact animals, restraint applied 6 h daily for 6 days increased plasma corticosterone, decreased significantly T and Prl, and, to a lesser degree, LH 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 specifically bound to crude testis membrane preparation, or the testicular responsiveness to hCG as measured by T levels 2 h after the injection of hCG (500 IU). In adr-x groups, a significant decrease in binding capacity of [125I]iodo-hCG and no alteration in hCG responsiveness have been observed. From these studies, it appears 1) that 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, 2) the sustained endogenous release of