Effects of circulating estradiol during rat estrous cycle on LH release following electrochemical stimulation of preoptic brain or administration of synthetic LRF.

Abstract

Serum levels of estradiol (E2) and LH during the 5-day rat estrous cycle were determined by radioimmunoassay (RIA). Serum E2 during the period between diestrus II and proestrus appeared to rise in a biphasic manner. The small and variable rise in serum E2 during diestrus II was followed by a marked rise (2–3- fold) at 0800 hr of proestrus I (day 3 postovulation). Thereafter E2 levels increased slowly through proestrus I until just prior to the surge of LH on proestrus II (day 4 postovulation). E2 levels declined asserum LH rose at 1800 hr of proestrus II. The temporal relationship between the circulating levelsof E2 during the estrous cycle and the release of LH after electrochemical stimulation(EC) of the medial preoptic area fMPOA) or administration of LH releasing factor (LRF) was next studied. Minimal increase in plasma LH was observed after EC stimulation of MPOA either during diestrus II when blood E2 values were low, or on morning of proestrus I when E2 levels were markedly elevated. However, with the extension of the period of exposure to elevated E2 levels, i.e., at 1800 hr of proestrus I or 1100 hrs of proestrus II, EC stimulation evoked marked increases in plasma LH. Intravenous administration of LRF (100 or 400 ng/rat) at all phases of the estrous cycleresulted in significant increases in plasma LH 15 min later, but a dose-related increase was significant only at proestrus II. As in the case of preoptic stimulation the smallest increase in plasma LH after LRF injection was noted at diestrus II and the greatest at proestrus II. During the intervening period, unlike that following preoptic stimulation, LH release after LRF administration increased along with the increase in titer and/or duration of exposure to E2. These results indicate that sensitivity of MPOA to EC stimulation and that of pituitary to LRF to raise plasma LH is closely related with the increment in circulating E2 during the estrous cycle, butthe time course of estrogen action may be different at these two loci. (Endocrinology94: 845, 1974)