Date of Award
In a cycling female rat, ovarian follicles produce steroid hormones under the influence of gonadotropin release from the pituitary gland. As the cycle of steroid synthesis and secretion increases, a spike in circulating estradiol drives an estrogen-positive feedback, which triggers luteinizing hormone (LH) and prolactin surges from the pituitary. As they circulate in the bloodstream, these hormones contribute to follicular steroidogenesis and luteolysis during the estrous cycle. Recent studies have supported the theory that estradiol circulating from ovarian origin also regulates the synthesis of neuroprogesterone in the hypothalamus, which is involved in the initiation of the LH surge. In order to test this theory as well as the neuroprogesterone effects on the prolactin surge, ovarectomized rats were treated with a known amount of estradiol sufficient enough to elicit the estrogen-induced prolactin and LH surges. The experimental group was treated with 50 nmol aminoglutethemide (AGT) through injection into the lateral ventricle of the brain, which inhibited the P450 side-chain cleavage necessary for steroid synthesis in the hypothalamus. Plasma samples were obtained over seven hours on the afternoon of the surge, and measured through radioimmunoassays for both prolactin and LH levels. Afternoon prolactin surges occurred in both vehicle and AGT-treatment rats, with peak values at 1500 hours. Prolactin levels tended to be lower with a delayed surge in the AGT-treatment group, although not significantly different from the vehicle-treatment group. LH levels were low and unchanged during the afternoon with no apparent surge in either the vehicle or AGT-treatment rats. These data do not support neuroprogesterone involvement in either estradiol-induced prolactin or LH surges.