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The caudal deficiencies of the Müllerian ducts (MDs) induced in chick embryos after early treatment with testosterone propionate (TP), 17 beta-estradiol benzoate (EB), or dihydrotestosterone (DHT) are the consequence of agenesia, i.e., a stop in duct development occurring during the sexually indifferent stage. The present work shows that EB and DHT act on the MDs in binding cellular estrogen receptors. Indeed, the antiestrogenic drug, tamoxifen, which competes with estrogens at the receptor site level, significantly decreases the percentage and extent of these MD caudal deficiencies. The results also show that such receptors are already present at a time when MDs begin to grow from 4.5 to 5 days of embryonic life onward. On the other hand, tamoxifen does not significantly modify agenesia induced by TP.
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