A quantitative analysis of the maturation of steroid negative feedbacks controlling gonadotropin release in the female rat: the infantile-juvenile periods, transition from an androgenic to a predominantly estrogenic control.

Abstract

To determine what ovarian or adrenal steroid(s) are involved in restraining gonadotropin secretion in infantile female rats, several experiments were performed. Adrenalectomy of 10-day-old rats markedly decreased serum progesterone (P) and, to a lesser extent, serum estradiol (E2) levels. Androgen (A) levels were only transiently reduced, and serum dihydrotestosterone was not affected. Serum LH and FSH, on the other hand, increased only transiently after adrenalectomy. Ovariectomy (OVX) failed to decrease serum P and partially depressed serum E2, but resulted in a marked fall of both testosterone (T) and dihydrotestosterone. Serum LH and FSH were increased in these animals. Replacement of pre-OVX serum T levels via Silastic capsules prevented the postcastration rise in both LH and FSH, suggesting that the increase in gonadotropins that follows OVX of 10-day-old rats is, to a large extent, a consequence of the loss of ovarian T. OVX of juvenile (27 days old) rats increased serum FSH and LH 48 h later and reduced both serum T and E2 levels, with no significant change in serum P. Replacement of pre-OVX serum T levels depressed post-OVX serum FSH and LH titers only partially. In contrast, replacement of pre-OVX serum E2 levels, effectively suppressed the postcastration rise in serum gonadotropins. The results suggest that 1) during the infantile period, gonadotropin release is predominantly under ovarian androgenic inhibitory control, but this mechanism is not very effective, because basal serum gonadotropin levels, particularly FSH, are elevated; 2) the effectiveness of the A negative feedback on FSH remains unchanged during prepubertal development; and 3) the previously reported increase in E2 negative feedback effectiveness that occurs after day 15 results in an E2 inhibitory signal that surpasses that of As, so that during juvenile days, most of the ovarian steroidal inhibitory control on gonadotropin release is mediated by E2.