ESTRADIOL REQUIREMENTS FOR INDUCTION AND MAINTENANCE OF THE GONADOTROPIN-RELEASING-HORMONE SURGE - IMPLICATIONS FOR NEUROENDOCRINE PROCESSING OF THE ESTRADIOL SIGNAL

Two experiments were performed to examine the temporal requirements of the estradiol signal for the GnRH and LH surges in the ewe. Hypophyse al portal and jugular blood (to measure GnRH and LH, respectively) wer e sampled from ewes set up in an artificial follicular phase model. Af ter progesterone withdrawal to simulate luteolysis, circulating estrad iol was raised to a preovulatory level by inserting estradiol implants , which then were removed at different times to vary estradiol signal duration. The objective of the first experiment was to assess the effe ct of withdrawing estradiol at surge onset on development and maintena nce of the GnRH/LH surges. Removal of estradiol, before surge onset, n either altered the LH surge in relation to that induced when the estra diol stimulus was maintained nor affected stimulation of a massive and sustained GnRH surge that outlasted the LH surge by many hours. Conti nued estradiol treatment, however, did prolong the GnRH surge. In the second experiment, the estradiol stimulus was shortened to test the hy pothesis that estradiol need not be present for the whole presurge per iod to induce GnRH/LH surges. Ewes received estradiol either up to the time of surge onset (21 h) or for periods equivalent to the last 14 h , the last 7 h, or the earliest 7 h of the 21-h signal. Shortening the signal to 14 h did not reduce its ability to stimulate a full GnRH su rge, but it did reduce the amplitude of the resultant LH surge. Furthe r shortening of the signal to 7 h, however, produced a mixed response. Most animals (8 of 10 combining the two 7-h groups) did not express G nRH surges. In the two ewes that did, GnRH surge amplitude and duratio n were again within the range observed with the 21-h estradiol signal, but the LH response was greatly reduced. These results indicate that, once the GnRH/LH surges of the ewe have begun, elevated estradiol is not required for surge maintenance. Development of a full GnRH surge r equires elevated estradiol for only a portion of the presurge period. More prolonged exposure to estradiol, however, is needed to maximize p ituitary responsiveness to GnRH. Since the estradiol signal for the Gn RH surge is relatively short (7-14 h) and temporally located well in a dvance of the surge itself, these results are consistent with the hypo thesis that estradiol is required only to activate the steroid-respons ive neuronal elements and not for progression of the signal from these elements to the actual surge process of GnRH release.