Abstract
(1) Estradiol benzoate (EB) at 250 μg when injected into hamsters at 12, 24, 48, 72, 96 or 120 hr after birth was equally effective at all times in suppression of sexual responsiveness measured as total lordosis duration (TLD) per 10 min test interval. (2) Testosterone propionate TP at 500 μg resulted in a significantly greater suppression in TLD when injected at 12, 24 or 48 hr as compared with injections at 72, 96 or 120 hr. (3) All neonatally injected female groups showed a significant reduction in TLD scores when compared with nontreated females with the exception of 96 hr TP treated females. (4) None of the neonatally treated male groups had TLD scores which were significantly different from the nontreated males. (5) All groups of treated females showed lordosis which in the 12- and 24-hr treatment groups did not change significantly as a result of castration or exogenous hormone treatment. (6) The 48-hr TP-treated females were the earliest treatment group in which the TLD score decreased significantly following ovariectomy and increased significantly following treatment with exogenous estrogen and progesterone. (7) Facilitation of lordosis followed by inhibition of lordosis on repeated progesterone injection (biphasic response) was not seen in hamsters of either sex injected with EB between 12 and 120 hr after birth. (8) The noninjected male hamsters and hamsters of both sexes receiving TP treatment at 96 hr or later showed a biphasic response to progesterone. (9) Our observations indicate that defeminization is most readily produced by estrogen treatment which in turn suggests that aromatization of androgen to estrogen is important for defeminization. (10) Since male hamsters respond to estrogen and progesterone, although with lower TLD scores than found for females, the male hamster is only partially defeminized either as a result of low androgen production and/or aromatization enzymes available during the critical stages of development.
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