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Department of Cell Biology, Physiology and Immunology, University of Córdoba, Córdoba, Spain
(Requests for offprints should be addressed to J E Sánchez-Criado, Section of Physiology, Faculty of Medicine, Avda. Menendez Pidal s/n, 14004 Córdoba, Spain; Email: fi1sacrj{at}uco.es)
Two-week ovariectomized (OVX) rats were injected over three days with 25 µg oestradiol benzoate (EB), 3 mg tamoxifen (TX) and 0.2 ml oil and their pituitaries were harvested for incubation experiments. Pituitaries from EB-and TX-treated OVX rats exhibited GnRH self-priming when incubated with their corresponding ligand. However, incubation of pituitaries with different ligands yielded divergent results: when pituitaries from EB-treated rats were incubated with 10–7 M TX they displayed GnRH self-priming, whereas incubation of pituitaries from TX-treated rats with 10–8 M oestradiol-17ß (E2) blocked GnRH self-priming. Further studies to analyse the latter finding revealed that: (a) E2 inhibited TX-induced GnRH self-priming in a dose-dependent manner while 10–8 M oestradiol-17
did not; (b) co-incubation of E2 with the pure anti-oestrogen ICI 182,780, but not with the selective oestrogen receptor modulator TX, reversed the E2 inhibitory effect; (c) the oestrogen receptor (ER)- selective agonist propylpyrazole triol, but not the ERß selective agonist diarylpropionitrile, mimicked the inhibitory effect of E2; (d) the analogue membrane-impermeable conjugated E2-BSA also inhibited TX-induced GnRH self-priming; and (e) a 15-min exposure of the pituitaries to E2 was sufficient to inhibit the GnRH self-priming elicited by TX. Although other explanations may exist, altogether these results suggested that E2, via an ER different from classical ER, inhibits the GnRH self-priming elicited by TX.
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