Effect of Castration and Steroid Replacement on Immunoreactive Gonadotropin-Releasing Hormone in the Hypothalamus and Preoptic Area*

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Abstract
The effect of castration alone or castration and subsequent administration of testosterone propionate to males or estradiol benzoate (EB) to females on the content and distribution of gonadotropin-releasing hormone (GnRH) in the median eminence and organum vasculosum of the lamina terminalis (OVLT) was studied in rats and mice. Specimens were labeled with the peroxidase-antiperoxidase method of imrnunocytochemistry using an antiserum to synthetic GnRH conjugated to bovine serum albumin. Five weeks after castration, the content of immunoreactive GnRH in the median eminence of rats and mice of both sexes was markedly depleted. The reduction in GnRH stores was most obvious in axons and nerve endings in the middle and caudal regions of the median eminence. Replacement therapy with gonadal steroids reversed the castrationinduced reduction in GnRH content. EB failed to completely restore GnRH in the median eminence of ovariectomized mice to control levels, but otherwise there were no differences in the effectiveness of replacement therapy with respect to sex or species. None of the experimental treatments had any effect on the distribution or content of GnRH associated with the OVLT. These observations suggest that: 1) after removal of the negative feedback action of gonadal steroids, there is an increased level of secretory activity by GnRH-producing neurons ending in the median eminence; 2) testosterone propionate in orchidectomized males and EB in ovariectomized females return the elevated secretory rate of such neurons to levels similar to those in intact control animals; and 3) GnRH neurons ending in the OVLT may not be directly involved in the negative feedback control of gonadotropin secretion. (Endocrinology 106: 1442, 1980)