Abstract
It was found that the implantation of 17-[beta]-estradiol on the tip of a fine glass capillary in the anterior median eminence-basal tuberal region inhibited the development of compensatory ovarian hypertrophy in rats. Daily control of the vaginal smear revealed that in the animals implanted with 17-[beta]-estradiol the number of cornification days had been decreased. Implantation of [DELTA]1[long dash]cortisone together with 17-[beta]-estradiol into the anterior median eminence-basal tuberal region resulted in a prevention of the estradiol suppressing action on compensatory ovarian hypertrophy in rats. [DELTA]1-cortisone implanted alone in the same area of the hypothalamus did not change the compensatory ovarian hypertrophy. It was concluded that the increasing gonadotropin secretion accompanied by compensatory ovarian hypertrophy is partly influenced by adrenocortical hormones too. This effect occurs as a modification of the estrogen feed-back mechanism and comes about on the level of the hypothalamus but, at the same time, it may be assumed that the steroids exert a direct influence on the pituitary level.