Regulation of Sex Differences in Progesterone Receptor Expression in the Medial Preoptic Nucleus of Postnatal Rats

Quadros, Princy S.; Goldstein, Alyssa; Vries, Geert J. De; Wagner, Christine K.

doi:10.1046/j.1365-2826.2002.00827.x

Cited by 56 publications

(41 citation statements)

References 62 publications

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“…In the rat, the female-typical profile of PR expression develops after birth. Thus ovariectomy on postnatal day 4 prevented the female-typical increase in PR levels observed between day 10 and 28 in the MPN [80]. Interestingly, preliminary results from our laboratory also suggest a role for postnatal estrogens in the development of PR in the female mouse.…”

Section: Reduced Female Sexual Behavior In Female Arko Micesupporting

confidence: 55%

“…We further propose that the feminizing action of estradiol normally occurs in genetic females between birth and the age of puberty (postnatal days [40][41][42][43][44][45][46][47][48][49][50]. Accordingly, several studies in which estrogen exposure was manipulated in both sexes during the perinatal developmental period have suggested that different critical periods exit for male-and female-typical organization of the brain [80,82]. Thus, prenatal exposure to estrogens induces the male-typical pattern of PR expression in the MPN and VMN, whereas postnatal exposure to estrogens leads to the female pattern of PR expression in these brain regions.…”

Section: Discussionmentioning

confidence: 99%

“…Our preliminary results (unpublished) indicated that gonadally intact ArKO females, which were not supplemented with any estrogens, show much lower levels of PR in the VMN than WT females. Whether the estradiol treatment used to induce female sexual receptivity in our previous study [8] [80]. Further studies are needed to determine whether the hormonal-neural circuitry of lordosis behavior has not been feminized in ArKO females and thus whether there is an active contribution of postnatal estradiol to the development of this circuit.…”

Section: Neural Mechanisms Potentially Affected In Female Arko Micementioning

confidence: 91%

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Role for estradiol in female-typical brain and behavioral sexual differentiation

Bakker

Baum

2008

Frontiers in Neuroendocrinology

170

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The importance of estrogens in controlling brain and behavioral sexual differentiation in female rodents is an unresolved issue in the field of behavioral neuroendocrinology. Whereas, the current dogma states that the female brain develops independently of estradiol, many studies have hinted at possible roles of estrogen in female sexual differentiation. Accordingly, it has been proposed that a-fetoprotein, a fetal plasma protein that binds estrogens with high affinity, has more than a neuroprotective role and specifically delivers estrogens to target brain cells to ensure female differentiation. Here, we review new results obtained in aromatase and a-fetoprotein knockout mice showing that estrogens can have both feminizing and defeminizing effects on the developing neural mechanisms that control sexual behavior. We propose that the defeminizing action of estradiol normally occurs prenatally in males and is avoided in fetal females because of the protective actions of a-fetoprotein, whereas the feminizing action of estradiol normally occurs postnatally in genetic females.

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Section: Reduced Female Sexual Behavior In Female Arko Micesupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: Neural Mechanisms Potentially Affected In Female Arko Micementioning

confidence: 91%

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Role for estradiol in female-typical brain and behavioral sexual differentiation

Bakker

Baum

2008

Frontiers in Neuroendocrinology

170

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“…In contrast, many characteristics cannot be differentiated by sex in adulthood because these sex differences are present only transiently during development [32, 54]. For example, around birth, male rats express much higher levels of progesterone receptor in the medial preoptic area than do females; this sex difference starts to disappear once the ovaries become active [55]. GABA B R gene expression exhibits similar characteristics.…”

Section: Discussionmentioning

confidence: 99%

Effect of Androgens on Sexual Differentiation of Pituitary Gamma-Aminobutyric Acid Receptor Subunit GABA<sub>B</sub> Expression

et al. 2004

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Previous work demonstrated a sexually dimorphic ontogenic expression of γ-aminobutyric acid receptors (GABA_BR) in rat pituitary. As sex steroids determine sex-specific expression patterns, we now studied the effect of sex hormones on pituitary GABA_BR expression. GABA_BR subunits, measured by Western blot and by semi-quantitative RT-PCR and luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone measured by RIA were determined in two experimental designs: First experimental design: 8- and 15-day-old females (8F, 15F); 8F and 15F treated with 100 µg testosterone propionate (TP) on day 1 of life (8F100TP, 15F100TP), 8- and 15-day-old males (8M, 15M) and 8M and 15M castrated on day 1 (8MC, 15MC). Second experimental design: 8-day-old female and male animals: 8F, 8F100TP, 8F treated with 1 µg/day TP on days 1–4 (8F1TP), 8F treated with the androgen antagonist Flutamide (Flut: 2.5 mg/100 g BW of pregnant mother on days E17-E23) (8F-Flut), 8M, 8MC, 8M treated with Flut as above (8M-Flut) and 8MC-Flut. In these animals, in addition, GABA, glutamate, aspartate and taurine were measured by HPLC in hypothalami and cortex. In the first set of experiments, GABA_B1R mRNA/protein expression was higher in 8F than in 15F, 8M or 15M. In 8F100TP, GABA_B1R mRNA/protein decreased to male levels. TP treatment did not alter GABA_B1R expression in 15F. There was no difference in GABA_B1R expression between 8M and 15M and neonatal castration did not modify its expression. In the second set of experiments, TP (1 µg) or Flut did not modify GABA_B1R in 8F, while 100 µg TP continued to decrease GABA_B1R expression. In 8M, Flut, alone or with castration, increased GABA_B1R mRNA/protein expression to 8F. Hypothalamic GABA content followed the same pattern as pituitary GABA_BR expression in 8-day-old animals, suggesting a cross-regulation. With regard to hormonal levels, 100 µg, but not 1 µg TP altered gonadotropins at 8 days, although both treatments effectively androgenized females as evidenced by lack of cycling. We conclude that androgens, acting pre- and postnatally, decrease pituitary GABA_BR subunit expression.

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“…The masculinization of the pattern of gonadotrophin release initially appears to be under the control of prenatally secreted testosterone, but postnatally both testosterone and oestradiol may be involved (Foecking et al 2005). Progesterone derived from either the maternal system or produced locally in the brain is also involved in CNS sexual differentiation and may be part of a cascade originating with testosterone and progressing to oestradiol and then progesterone to induce full masculinization (Quadros et al 2002a). …”

Section: Steroid Control Of Brain-regulated Functions and Behaviourmentioning

confidence: 99%

The control of sexual differentiation of the reproductive system and brain

Wilson¹,

Davies²

2007

Reproduction

160

116

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This review summarizes current knowledge of the genetic and hormonal control of sexual differentiation of the reproductive system, brain and brain function. While the chromosomal regulation of sexual differentiation has been understood for over 60 years, the genes involved and their actions on the reproductive system and brain are still under investigation. In 1990, the predicted testicular determining factor was shown to be the SRY gene. However, this discovery has not been followed up by elucidation of the actions of SRY, which may either stimulate a cascade of downstream genes, or inhibit a suppressor gene. The number of other genes known to be involved in sexual differentiation is increasing and the way in which they may interact is discussed. The hormonal control of sexual differentiation is well-established in rodents, in which prenatal androgens masculinize the reproductive tract and perinatal oestradiol (derived from testosterone) masculinizes the brain. In humans, genetic mutations have revealed that it is probably prenatal testosterone that masculinizes both the reproductive system and the brain. Sexual differentiation of brain structures and the way in which steroids induce this differentiation, is an active research area. The multiplicity of steroid actions, which may be specific to individual cell types, demonstrates how a single hormonal regulator, e.g. oestradiol, can exert different and even opposite actions at different sites. This complexity is enhanced by the involvement of neurotransmitters as mediators of steroid hormone actions. In view of current environmental concerns, a brief summary of the effects of endocrine disruptors on sexual differentiation is presented.

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Regulation of Sex Differences in Progesterone Receptor Expression in the Medial Preoptic Nucleus of Postnatal Rats

Cited by 56 publications

References 62 publications

Role for estradiol in female-typical brain and behavioral sexual differentiation

Role for estradiol in female-typical brain and behavioral sexual differentiation

Effect of Androgens on Sexual Differentiation of Pituitary Gamma-Aminobutyric Acid Receptor Subunit GABA<sub>B</sub> Expression

The control of sexual differentiation of the reproductive system and brain

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