Female rats were killed during the days encompassing the first ovulation (32–38 days of age) and classified in different phases of puberty, according to criteria previously established. Serum estradiol (E2) levels were low in anestrus (A) and the initial part of early proestrus (EP-1), increased during the late part of early proestrus (EP-2), and reached the highest values on the morning of the preovulatory surge of gonadotropins [late proestrus phase (LP)]. By the next day [estrus (E)], Ej levels had returned to basal values. Progesterone (P) levels were low in A, started to increase in EP-1, and reached peak levels in EP-2. At LP, although still elevated, P titers were somewhat lower than those in EP-2. After the first ovulation, levels increased markedly, reaching the highest values on the day of the first diestrus (D1). Serum androgens (testosterone and dihydrotestosterone) increased slightly throughout puberty. In vitro ovarian E2 and P responsiveness to hCG increased dramatically between A and LP, the first significant change being observed between A and EP-1. After ovulation had occurred, (E and Di phases of puberty) E2 responsiveness declined precipitously, whereas that of P remained elevated. Basal in vitro release of E2 increased gradually between A and LP and declined thereafter. Basal release of P increased during E and D2. Ovarian androgen response to hCG declined markedly between A and E, remaining low at D1. Ovarian prostaglandin E (PGE) release in response to hCG increased 2-fold between A and EP-2 and decreased abruptly during E, a time at which basal release was greatly enhanced. By D1, the response was still blunted and the basal PGE levels were elevated. Significant correlations were found between uterine weights and both serum E2 levels and E2 released in vitro in response to hCG at different phases of puberty. It is suggested that 1) the increase in serum E2 and P that antecedes the first preovulatory surge of gonadotropins is caused by an enhancement in ovarian responsiveness to low circulating gonadotropin levels, 2) P may play an important role in facilitating the expression of the positive feedback of estrogen at puberty, and 3) the observed changes in ovarian responsiveness to hCG are not mediated through PGE release, which, however, may participate in inducing luteinization of the ovulatory follicles.
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