Transition of the Rabbit Corpus Luteum to Estrogen Dependence during Early Luteal Development*

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Abstract
The early development of the rabbit corpus luteum shifts by day 6 postcoitum from a period of estrogen independence to one of estrogen dependence. The nature of this transition was explored. Ectopic corpora lutea were established in rabbits by autotransplanting preovulatory follicles to the kidney 6.5-8.0 h after mating (day 0). At this time, the rabbits were bilaterally ovariectomized. To determine whether estradiol might be produced transiently by the developing corpora lutea or by an extraovarian source, estradiol concentrations were measured in peripheral blood and in renal blood. The concentration of estradiol in peripheral blood did not vary significantly through day 4 of development, and, on each day, averaged less than 1.2 pg/ml. No significant differences were observed between the concentrations of estradiol in peripheral blood, in blood draining the kidney bearing ectopic corpora lutea, or in blood from the contralateral kidney. The early development of ectopic corpora lutea occurs in an extremely low estradiol environment. When silastic capsules containing estradiol were inserted into these rabbits on day 3 or 5, serum progesterone rose steadily to .apprx. 6 ng/ml by day 10. If estradiol implants were not inserted until day 6 or 7, serum progesterone began to level off by day 5 and then to fall. This decline in progesterone was reversed within 24 h after insertion of the implants, suggesting that no substantial lag period is required for the expression of estradiol action. Days 5-6 represent a critical period for the corpus luteum, during which estradiol must be present for continued luteal development and secretion of progesterone. Estradiol binding to the cytosol and nuclear fractions from ectopic corpora lutea was low on day 3, increased significantly by day 5, and had fallen by day 6. The day of highest estradiol binding corresponds to the day which marks the transition from estrogen independence to estrogen dependence.

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