[The GnRH precursor is present in the anterior pituitary gland and an important increase of its content precedes serum LH surge induced by estradiol-17 beta in female primates].

Estradiol-17 beta (E2 17 beta) is well known to evoke a preovulatory-like LH surge in ovariectomized monkeys even in the absence of the integrity of the hypothalamo-pituitary connections. LH release from the anterior pituitary (AP) is reliant on stimulation by hypothalamic GnRH which is derived from proteolytic cleavage of a precursor (designated Pro-GnRH-GAP) which also results in the production of an associated peptide (GAP). The present study examined the effects of E2 17 beta on the hypothalamic content of Pro-GnRH-GAP, GnRH and GAP while incidental observations revealed the presence of Pro-GnRH-GAP and its products in the AP. Changes in GnRH and GAP were closely related at all times after E2 17 beta treatment. However, the pattern of change in the hypothalamus and AP was inversely related. Pro-GnRH-GAP levels remained unchanged in the hypothalamus whereas in the AP the peptide increased markedly (48 hrs. post E2 17 beta) prior to the LH surge and declined to low levels (72 hrs. post E2 17 beta) at the time of the LH surge. The increase in Pro-GnRH-GAP in the AP that precedes the rise in GnRH and accompanying LH surge by 24 hrs. strongly indicates that AP GnRH is more important than hypothalamic GnRH for the mediation of the E2 17 beta-induced LH surge in female primate.