Responses of Serum LH and FSH to the Removal of Steroid Feedback Inhibition

Abstract

Sex differences in the serum gonadotropin responses to the removal of feedback inhibition were studied in rats which had been given chronic implants of testosterone (T) capsules at the time of castration. Following capsule removal, serum LH increased significantly within 24 h in males, but only after 3 or 4 days in females. Adult females, sterilized with a single injection of 10 μg of testosterone propionate (TP) on postnatal day 3, 4, or 5, showed a rapid ‘male-like’ LH response to removal of the T capsules. However, the rise in circulating LH after capsule removal in adult females treated with 500 μg of TP on day 4 of age was even slower than that observed in control females. The pituitary LH responses to a single intravenous injection of LHRH were similar in androgenized and control females when tested after castration; however, a significantly impaired response was seen in the 500-μg TP females during T treatment. Although the T capsules used in these studies suppressed circulating LH in control and androgenized females, basal serum FSH titers 3 weeks after ovariectomy and T-capsule implantation, especially in the low-dose androgenized females, were significantly elevated when compared with intact values. Reliable sex differences were not observed in the FSH response to T-capsule removal. To examine the neural control of the ‘postcastration’ response of circulating gonadotropins, male and female rats were subjected to anterior deafferentation of the hypothalamus (AD) at the time of gonadectomy and T-capsule implantation. 3 weeks later, the capsules were removed. The LH response to T-capsule removal was similar in AD and sham-cut males, with significant increases being observed after 1 day. Plasma LH titers in the AD females paralleled those of the sham-cut females, with neither group showing a sustained increase until 3 days after T-capsule removal. These findings indicate that the rapid LH response to the removal of feedback inhibition which is characteristic of males, can be induced in females by neonatal, low-dose androgen treatment. A high dose of androgen administered neonatally did not masculinize the LH response to the removal of feedback inhibition possibly due to a disruptive effect on the hypothalamic-pituitary axis. In addition, the anterior inputs to the medial basal hypothalamus, which are necessary for cyclic gonadotropin secretion in female rats, do not appear to be responsible for sex differences in the ‘postcastration’ LH response.