Effects of Hypothalamic and Hypophysial Estrogen Implants on Pituitary and Plasma LH in Ovariectomized Rabbits

Effects exerted by localized hypothalamic and hypophysial implants of minute amounts of estradiol benzoate on pituitary and plasma LH were studied with the use of the ovarian ascorbic acid depletion method (OAAD). In control ovariectomized rabbits the pituitary LH content measured 0.53 ±0.05 μg/mg- When estrogen was implanted in the posterior median eminencebasal tuberal region of the hypothalamus (PME), the pituitary LH content was reduced to less than 0.1 μg/mg in 5 of 7 rabbits. However, when estrogen was implanted in other parts of the hypothalamus, it failed to depress pituitary LH (0.51 ±0.06 μg/mg). With estrogen in the anterior hypophysis, the pituitary LH content was also somewhat lowered (0.34 ±0.03 μg/mg). The castration level of plasma OAAD, an indicator of plasma LH content, was 21.6 ± 3.3 % as compared with the normal (noncastrate) level of 5.8 ±0.9%. Estrogen implants in PME inhibited the postcastration elevation in plasma OAAD (9.1 ±3.4%), whereas implants in other parts of the hypothalamus were ineffective (plasma OAAD, 24.1 ±2.5%). The plasma OAAD level in animals with estrogen implanted in the anterior hypophysis was even higher (34.2 ±1.8%) than in the castrate controls. Estrogen implantation into PME resulted in a doubling of the weight of the hypophysis, whereas similar effects were not observed following implantation into other parts of the hypothalamus or directly into the anterior hypophysis. The results indicate that estrogen acts on PME in such a way as to inhibit synthesis of pituitary LH and thereby to prevent the postovariectomy rise in plasma LH, while at the same time stimulating hypertrophy of the hypophysis. Acting directly on the anterior hypophysis, estrogen appears to activate release of LH into the circulation, where it is reflected in elevated plasma OAAD. (Endocrinology75: 579, 1964)