Postnatal development of sensitivity to estrogen and androgen in male, female and psuedohermaphroditic guinea pigs

Authors

  • Robert W. Goy,

    1. Department of Reproductive Physiology and Behavior, Oregon Regional Primate Research Center, Beaverton, Oregon, and University of Kansas, Lawrence, Kansas
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  • Charles H. Phoenix,

    1. Department of Reproductive Physiology and Behavior, Oregon Regional Primate Research Center, Beaverton, Oregon, and University of Kansas, Lawrence, Kansas
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  • Richard Meidinger

    1. Department of Reproductive Physiology and Behavior, Oregon Regional Primate Research Center, Beaverton, Oregon, and University of Kansas, Lawrence, Kansas
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    • Now in the United States Air Force.


  • Publication no. 211 of the Oregon Regional Primate Research Center supported in part by grant FR 00163 of the National Institutes of Health and in part by research grants MH 504 and 08634 from the National Institute of Mental Health, United States Public Health Service.

Abstract

Lordosis responses on the day of birth were measured in female pseudohermaphrodites, their male siblings, and control females and males. All subjects displayed lordosis. Differences in average duration of the response were not significant.

Relationships between exogenous estrogen and display of lordosis at later ages were studied in gonadectomized subjects. At seven days, estrogen did not induce lordosis in any subject. All normal females displayed lordosis at 21, 35, 60, and 90 days, and estrogen-sensitivity increased steadily. Pseudohermaphrodites failed to respond to hormones until 35 days, and responses were infrequent and abbreviated. Age at time of ovariectomy did not influence performance of pseudohermaphrodites. Males showed lowest responsiveness to estrogen over all ages.

Pseudohermaphrodites resembled the male in postnatal responsiveness to androgen. Although postnatal testosterone induced mounting behavior in normal females, pseudohermaphrodites, like males, displayed more mounting and mounted at earlier ages.

Results suggest that prenatal androgen has not impaired the neural mechanism for lordosis at birth. Rather it acts to alter, during the fetal stage, the mechanism which normally directs the development of estrogen-sensitivity of the neural mechanism in the genetic female. Additionally, prenatal androgen lowers the hormonal threshold for mounting behavior.

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