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Gonadal steroids are thought to act by activation of the genome following cytoplasmic binding, translocation of the hormone--receptor complex to the nucleus and chromatin binding at specific acceptor sites. This study examined the kinetics of chromatin binding of estradiol by hypothalamic and cortical cells of adult gonadectomized male and female rats. In both sexes binding was found to be limited to hypothalamic cells. The kinetics of binding differed between the sexes, estradiol being retained less well in males. In females hypothalamic chromatin binding was shown to be of limited capacity and to be competitively inhibited by unlabeled estradiol. Unlabeled testosterone inhibited estradiol binding when administered subcutaneously 3 h before the estradiol, but not by testosterone when administered either intravenously or concurrently with the estradiol. It was suggested that the observed sex difference in hypothalamic chromatin binding might underlie the relative insensitivity of the male to the lordosis-inducing properties of estradiol.
R E Whalen, and
K L Olsen
January 1974,
Neuroendocrinology,
R E Whalen, and
K L Olsen
February 1974,
Brain research,
R E Whalen, and
K L Olsen
January 1981,
Ontogenez,
R E Whalen, and
K L Olsen
May 1971,
Endocrinology,
R E Whalen, and
K L Olsen
June 1978,
Endocrinologia experimentalis,
R E Whalen, and
K L Olsen
January 1983,
Problemy endokrinologii,
R E Whalen, and
K L Olsen
January 1985,
Ontogenez,
R E Whalen, and
K L Olsen
November 1983,
Life sciences,
R E Whalen, and
K L Olsen
August 1989,
Neuroendocrinology,
R E Whalen, and
K L Olsen
January 1982,
Neurochemistry international,
