Content of Luteinizing Hormone-Releasing Factor and Luteinizing Hormone During the Estrous Cycle and After Changes in Gonadal Steroid Titers

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Abstract
LH-releasing activity of acidic extracts of the stalk-median eminence region was estimated by the ovarian ascorbic acid depletion induced by intravenous injection of the extracts into immature test rats pretreated with gonadotrophins. In cycling females, LH-releasing activity was highest in the evening of late diestrus, and it declined at proestrus. Castration of either males or females produced no significant changes in the hypothalamic content of LH-RF. Treatment for 14 days with varying doses of estradiol benzoate in females and testosterone propionate in males was also ineffective in altering the content of the releasing factor, except for a large dose (1000 μg) of testosterone propionate which caused a slight decline in activity in males. Both estradiol and testosterone lowered hypophysial LH content. Implants of testosterone and estradiol into the median eminence region, which were effective in altering gonadotrophin secretion, also lowered the content of stored LH-RF. Implants of testosterone in the hypophysis failed to evoke detectable changes in gonadotrophin secretion or to alter the content of LH-RF. By contrast, estradiol implanted in the anterior pituitary altered gonadotrophin secretion and caused an elevation in the content of LH-RF. The results suggest that the LH-RF may play a role in the regulation of LH secretion, and indicate that gonadal steroids can act on both the hypothalamus and anterior pituitary to modify LH secretion. A hypothesis is advanced involving negative feedback of both gonadal steroids and LH on the hypothalamus to explain the failure of castration and systemic administration of gonadal steroids to alter LH-RF content. (Endocrinology76: 700, 1965)

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