Circulating estradiol and the activation of male and female copulatory behavior in Japanese quail (Coturnix japonica) |
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Authors: | J T Watson M Abdelnabi S Wersinger M A Ottinger E Adkins-Regan |
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Affiliation: | Department of Psychology, Cornell University, Ithaca, New York 14853. |
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Abstract: | Previous experiments using systemic and preoptic area (POA) hormone treatments have shown that aromatization of testosterone (T) to estrogen (E) is essential for activation of male-typical copulatory behavior in castrated male Japanese quail (Coturnix japonica). Two experiments were conducted to determine whether circulating estrogen levels characteristic of normal intact males are high enough to activate male-typical or female-typical copulatory behavior. In Experiment 1, blood samples were drawn every 4 hr from groups of sexually active male quail housed under a 16L:8D light-dark cycle, and assayed for estradiol (E2) concentration. The mean +/- SEM serum E2 was 54.2 +/- 3.6 pg/ml, and no daily cycle in serum E2 was seen. The males were then tested for sexual behavior; 88% mounted females, and 23% crouched when mounted by males. In Experiment 2, 51 males were castrated and implanted with Silastic tubes containing estradiol benzoate (EB) and/or cholesterol designed to produce five different levels of serum E2, then tested for male- and female-typical copulatory behavior and bled. The serum E2 in EB-implanted quail which mounted (253 +/- 30 pg/ml) was significantly higher than that of intact quail in Experiment 1, and only 10.2% of intact males had serum E2 as high as the minimum associated with mounting in EB-implanted males. These results show that serum E2 levels in intact males are not high enough to support male-typical copulation, and that aromatization in the POA to produce locally high E2 levels may be required. In addition, it was found that the threshold serum E2 to elevate receptivity significantly was 3.6 times the intact male level, and only slightly higher than serum E2 reported for intact females. Thus the lack of receptivity in intact males is probably due to insufficient circulating E2, and the male is not defeminized with respect to sensitivity to E2 for activation of receptivity. |
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