A combination of in vivo and in vitro experiments are designed to examine the HYPOTHESIS that ESTROGEN induces the LH surge by activating release of norepinephrine and stimulating release of LHRH. Immunocytochemistry and electron microscopy will be used to examine dopamine-beta-hydroxylase (DBHJ) immunopositve terminals in the,vicinity of LHRH neurons. Parameters of DBH terminals will be measured using images directly digitized with a TV camera in the electron microsope. Number and size of terminals, number of vesicles and proximity to LHRH neurons will be measured in digitized images and statistically analysed to evaluate the role of putative norepinephrine release in the induction of the surge of luteinizing hormone necessary for ovulation. Animal models will include: - 1) spontaneous ovulators with a luteal phase, guinea pigs; 2) induced ovulators, ferrets; 3) seasonal ovulators, bats; and 4) once only ovulators, lamprey. In addition, the HYPOTHESIS that estrogen promotes the cdnversion of high molecular weight LHRH precursors to mature forms will be the focus of HPLC separation and RIA quantitation of large molecular weight forms of LHRH, i.e. precursors, and active, mature hormone. The HYPOTHESIS that estrogen modulates the levels of other forms of LHRH decapeptide, i.e., lamprey-like LHRH, in mammals will also be examined by HPLC and RIA. These other non-mammalian forms of LHRH may function not as neuroendocrine, but as neuromodulatory agents. Finally, in vitro-perifusion will be used to further examine the HYPOTHESIS that estrogen induces the release of LHRH via noradrenergic mechanisms by examining the release of LHRH induced by estrogen in the presence of opiates.
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