Independent and overlapping effects of corticosterone and testosterone on corticotropin-releasing hormone and arginine vasopressin mRNA expression inthe paraventricular nucleus of the hypothalamus and stress-induced adrenocorticotropic hormone release

Adrenocorticotropin (ACTH) release is regulated by both glucocorticoids and androgens; however, the precise interactions are unclear. We have controll ed circulating corticosterone (B) and testosterone (T) by adrenalectomy (AD X) +/- B replacement and gonadectomy (GDX) +/- T replacement, comparing the se to sham-operated groups. We hoped to reveal how and where these neuroend ocrine systems interact to affect resting and stress-induced ACTH secretion . ADX responses. In gonadal-intact rats, ADX increased corticotropin-releasin g factor (CRH) and vasopressin (AVP) mRNA in hypothalamic parvocellular par aventricular nuclei (PVN) and ACTH in pituitary and plasma. B restored thes e toward normal. GDX blocked the increase in AVP but not CRH mRNA and reduc ed plasma, but not pituitary ACTH in ADX rats. GDX+T restored increased AVP mRNA in ADX rats, although plasma ACTH remained decreased. Stress responses. Restraint-induced ACTH responses were elevated in ADX gon adally intact rats, and B reduced these toward normal. GDX in adrenal-intac t and ADX+-B rats increased ACTH responses. Without B, T did not affect ACT H; together with B, T restored ACTH responses to normal. The magnitude of A CTH responses to stress was paralleled by similar effects on the number of c-fos staining neurons in the hypophysiotropic PVN. We conclude that gonadal regulation of ACTH responses Po ADX is determined by T dependent effects on AVP biosynthesis, whereas CRH biosynthesis is B-d ependent. Stress-induced ACTH release is not explained by B and T interacti ons at the PVN, but is determined by B- and T-dependent changes in drive to PVN motorneurons.