Role of Estrogens and Progestins in the Development of Female Sexual Behavior Potential

Hendricks, Shelton E.

doi:10.1007/978-1-4899-2453-7_4

Cited by 8 publications

(11 citation statements)

References 140 publications

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“…However, these nonandrogenic steroids are less likely than androgens to cause masculinization. Although very high doses of progesterone have been reported to cause defeminization in rodents (see Hendricks, 1992), typically these hormones demasculinize or have no effect (Hendricks, 1992;Shapiro, Goldman, Bongiovanni, & Marino, 1976).…”

Section: Summary and Conclusion For Hypothesismentioning

confidence: 99%

Human behavioral sex differences: A role for gonadal hormones during early development?

Collaer

Hines²

1995

Psychological Bulletin

691

450

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Evidence that gonadal hormones during prenatal and neonatal development influence behavior is reviewed. Several theoretical models of hormonal influences, derived from research in other species, are described. These models are evaluated on the basis of data from humans with either normal or abnormal hormonal exposure. It is concluded that the evidence is insufficient to determine which model best explains the data. Sexual differentiation may involve several dimensions, and different models may apply to different behaviors. Gonadal hormones appear to influence development of some human behaviors that show sex differences. The evidence is strongest for childhood play behavior and is relatively strong for sexual orientation and tendencies toward aggression. Also, high levels of hormones do not enhance intelligence, although a minimum level may be needed for optimal development of some cognitive processes. Directions for future research are proposed.

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Section: Summary and Conclusion For Hypothesismentioning

confidence: 99%

Human behavioral sex differences: A role for gonadal hormones during early development?

Collaer

Hines²

1995

Psychological Bulletin

691

450

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show abstract

“…Lisk and Suydam (1967) likewise conclude that "feminization appears to be the neutral condition" (p. 182). Yet researchers have previously suggested that estrogen (presumably of ovarian origin) may play an active role in feminization of the brain (e.g., Döhler 1991;Döhler et al 1984b;Hendricks 1992;Toran-Allerand 1976;. Toran-Allerand, for example, performed a series of in vitro studies in 1976 and concluded that "these .…”

Section: Female Developmentmentioning

confidence: 99%

A role for ovarian hormones in sexual differentiation of the brain

Fitch¹,

Denenberg²

1998

Behav Brain Sci

159

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Historically, studies of the role of endogenous hormones in developmental differentiation of the sexes have suggested that mammalian sexual differentiation is mediated primarily by testicular androgens, and that exposure to androgens in early life leads to a male brain as defined by neuroanatomy and behavior. The female brain has been assumed to develop via a hormonal default mechanism, in the absence of androgen or other hormones. Ovarian hormones have significant effects on the development of a sexually dimorphic cortical structure, the corpus callosum, which is larger in male than in female rats. In the females, removal of the ovaries as late as Day 16 increases the cross-sectional area of the adult corpus callosum. Treatment with low-dose estradiol starting on Day 25 inhibits this effect. Female callosa are also enlarged by a combination of daily postnatal handling and exogenous testosterone administered prior to Day 8. The effects of androgen treatment are expressed early in development, with males and testosterone-treated females having larger callosa than control females as early as Day 30. The effects of ovariectomy do not appear until after Day 55. These findings are more consistent with other evidence of a later sensitive period for ovarian feminization as compared to androgenic masculinization.

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“…The prenatal hormonal exposure has been proposed to account for the development of individual variations in phenotype among males and females (vom Saal, 1982;vom Saal & Bronson, 1980a,b). The fact that the females in the present study showed signs of feminization and defeminization simultaneously after prenatal treatment with antiestrogen may suggest that the defeminization seen normally in untreated females could be the price paid to achieve normal development of reproductive functions that are organized by prenatal hormones (but see Hendricks, 1992;Collaer & Hines, 1995).…”

Section: Discussionmentioning

confidence: 73%

“…Furthermore, administration of antiestrogen neonatally impaired the formation of corpora lutea and reduced lordosis behavior in adulthood in response to estradiol benzoate (EB) and progesterone (P) (Döhler, Hancke, et al ., 1984;Etgen & Whalen, 1979). These reports suggest that estrogen may in fact be involved in actively feminizing the female (Hendricks, 1992;Collaer & Hines, 1995). Studies of knockout animals lacking the estrogen receptor alpha, beta or both (ER) reported complete infertility in both sexes, absence of breast tissue development, precocious maturation of the ovary, absence of corpora lutea and development of structures resembling the seminiferous tubules of the testis in the ovary Couse et al ., 1999;Krege et al ., 1998).…”

mentioning

confidence: 99%

Enhanced feminine sexual behavior and infertility in female rats prenatally treated with an antiestrogen

Matuszczyk¹

2003

Scandinavian J Psychology

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An attempt to elucidate the possible role of prenatal estrogen on the development of feminine sexual behavior and reproductive function was made by treating females with the antiestrogen CI628 prenatally on days 13-19. Control females were prenatally treated with saline or remained untreated. The animals were delivered by caesarian section on day 22 of pregnancy and placed with foster mothers whose newborn pups had been previously removed. Intact peripubertal females in each treatment group were observed for several reproductive measures, including the capacity to become pregnant. Other females were ovariectomized in adulthood and treated with estradiol benzoate (EB) (1, 1.5, 2 or 4 micro g/rat) and 0.5 mg progesterone and tested for receptivity, proceptivity and sexual partner preference. Two weeks after the completion of these tests, the females were injected daily for 7 days with 0.25 mg testosterone and tested for sexual partner preference and mounting behavior. The results obtained showed accelerated vaginal opening, and infertility in the antiestrogen-treated intact females and enhanced receptivity and proceptivity in response to 1 micro g EB in the antiestrogen ovariectomized females. Sexual partner preference and mounting behavior did not differ between groups. These results suggest an involvement of prenatal estrogen on the development of female reproductive function, but not on behavioral differentiation.

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Role of Estrogens and Progestins in the Development of Female Sexual Behavior Potential

Cited by 8 publications

References 140 publications

Human behavioral sex differences: A role for gonadal hormones during early development?

Human behavioral sex differences: A role for gonadal hormones during early development?

A role for ovarian hormones in sexual differentiation of the brain

Enhanced feminine sexual behavior and infertility in female rats prenatally treated with an antiestrogen

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