Ovarian Steroid Regulation of Estrogen and Progesterone Receptor Messenger Ribonucleic Acid in the Anteroventral Periventricular Nucleus of the Rat

Simerly, Richard B.; Carr, Andrew; Zee, Michele C.; Lorang, Dominique

doi:10.1111/j.1365-2826.1996.tb00685.x

Cited by 125 publications

(82 citation statements)

References 70 publications

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“…Because most brain areas require estrogen receptor activation for induction of P receptor synthesis (Bogic et al, 1988;Simerly et al, 1996;Shughrue et al, 1997;Camacho-Arroyo et al, 1998;Allan et al, 2001), blunted CRF-enhanced startle after acute P injection without estrogen priming suggests this probably was not mediated through the P receptor. This is corroborated by results from the chronic P replacement study.…”

Section: Discussionmentioning

confidence: 99%

Progesterone Attenuates Corticotropin-Releasing Factor-Enhanced But Not Fear-Potentiated Startle via the Activity of Its Neuroactive Metabolite, Allopregnanolone

Toufexis¹,

Davis²,

Hammond³

et al. 2004

J. Neurosci.

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Intact female rats and ovariectomized (OVX) rats with different ovarian steroid replacement regimens were tested for changes in corticotropin-releasing factor (CRF)-enhanced startle (increased acoustic startle amplitude after intracerebroventricular infusion of 1 g of CRF). OVX rats injected with estradiol (E) followed by progesterone (P) showed a blunted CRF-enhanced startle effect compared with OVX and E-injected rats. CRF-enhanced startle also was reduced significantly in lactating females (high endogenous P levels) compared with cycling rats (low to moderate P levels), as well as in non-E-primed rats when P was administered acutely (4 hr before testing) or chronically (7 d P replacement). The ability of P to attenuate CRF-enhanced startle was probably mediated by its metabolite allopregnanolone [tetrahydroprogesterone (THP)], because THP itself had a similar effect, and chronic administration of medroxyprogesterone, which is not metabolized to THP, did not blunt CRF-enhanced startle but instead slightly increased it. These data suggest that P blunts CRF-enhanced startle through a mechanism involving its neuroactive metabolite THP, although a role for the P receptor cannot be completely ruled out. Finally, neither chronic P replacement nor acute THP affected fear-potentiated startle, suggesting that P metabolites have an effect on the bed nucleus of the stria terminalis and anxiety rather than on the amygdala and stimulus-specific fear.

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Section: Discussionmentioning

confidence: 99%

Progesterone Attenuates Corticotropin-Releasing Factor-Enhanced But Not Fear-Potentiated Startle via the Activity of Its Neuroactive Metabolite, Allopregnanolone

Toufexis¹,

Davis²,

Hammond³

et al. 2004

J. Neurosci.

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“…Prog receptors in the AvPv, a region that sends projections to the mPOA (Pfaff & Schwartz-Giblin 1998, Simerly et al 1996, play an indispensable part in the timing mechanism for the LH surge (Chappell et al 1999). As such, AvPv PRs also influence female sex behavior (Chappell & Levine 2000, Levine et al 2001, Hahn & Coen 2006.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic progesterone receptor-A mediates gonadotropin surges, self priming and receptivity in estrogen-primed female mice

White

Sheffer²,

Teeter³

et al. 2007

Journal of Molecular Endocrinology

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Ovarian progesterone (Prog) is an essential steroid hormone for the secretion of GnRH and reproductive behavior. It exerts primary effects through the progesterone receptor (PR). When analyzed separately in vitro, PR isoforms (PR-A, PR-B) display striking differences in transcriptional activity. The present study was undertaken to determine the in vivo impact of each isoform on hypothalamic function in female mice with ablation of a single isoform, either PR-A or PR-B. To this end, we used single-cell RNA analyses, reverse transcriptase real-time (q)PCR mRNA analyses of punched-out tissue, immunohistochemistry, and reproductive behavior. We provide evidence for the requirement of PR-A in individual ventrolateral ventromedial nucleus (vlVMN) neurons for Prog-facilitated proceptive and receptive behaviors in estrogen benzoate (EB)-primed females and the reciprocal male interactions. We clarify histological and molecular mechanisms of PR isoform activity by showing that (1) PR-A is predominant in individual vlVMN neurons controlling female lordosis circuitry, whilst (2) PR-B is predominant in those VMN subdivisions that provide for amplification of PR-A activity. We go on to demonstrate that PR-A is dominant in the anteroventral periventricular nucleus but not the arcuate nucleus that feed fibers into and around the VMN. In the medial preoptic area, high levels of GnRH RNA in EB-primed PR-A-expressing mice were seen coincident with increased plasma LH levels. Two consecutive GnRH pulses enhanced LH only in primed PR-A-expressing females. In all, the findings are consistent with the hypothesis that hypothalamic PR-A-mediated genomic activities result in reproductive behavior coordinated with ovulation.

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“…1) was selected for statistical evaluation because the level of PR mRNA in this brain region is highly sensitive to estrogenic action and has been well characterized (6,12). Relative optical density measurements of PR hybridization signal were obtained from film autoradiograms with a computer-based image analysis system (C-Imaging, Pittsburgh).…”

Section: Methodsmentioning

confidence: 99%

Responses in the brain of estrogen receptor α-disrupted mice

Shughrue

Lubahn

Negro‐Vilar

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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These studies sought to determine if neurons in the estrogen receptor-␣ knockout (ER␣KO) mouse brain concentrated 16␣-[ 125 I]iodo-11␤-methoxy-17␤-estradiol ( 125 I-estrogen), and if so, whether estrogen binding augmented the expression of progesterone receptor (PR) mRNA. Mice were injected with 125 I-estrogen and cryostat sections thaw mounted onto emulsion-coated slides. After 30-90 days of exposure, cells with a nuclear uptake and retention of 125 Iestrogen were observed in a number of ER␣KO mouse brain regions including the preoptic nucleus and arcuate nucleus of the hypothalamus, bed nucleus of the stria terminalis, and amygdala, although the number of labeled cells and intensity of nuclear concentration was markedly attenuated when compared with wild-type littermates. Competition studies with excess 17␤-estradiol, diethylstilbestrol, or moxestrol, but not with R5020 or dihydrotestosterone, prevented the nuclear concentration of 125 I-estrogen. To determine if the low level of estrogen binding was capable of regulating gene expression, in situ hybridization was used to evaluate PR mRNA in the brain. ER␣KO and wild-type mice were ovariectomized and treated with vehicle or 17␤-estradiol, and brains were sectioned and hybridized with a PR cRNA probe. Analysis of hybridization signal revealed a similar, low level of PR mRNA in ovariectomized wild-type and homozygous mice, and a marked increase in expression after treatment of ovariectomized animals with 17␤-estradiol, with the level of hybridization signal being significantly higher in wild-type animals when compared with ER␣KO mice. The results demonstrate that estrogen binds in the ER␣KO brain and is capable of modulating PR gene expression, thus supporting the presence and functionality of a nonclassical estrogen receptor.Estrogen is known to act in discrete regions of the female brain to regulate gamete production, proceptive and receptive behaviors, and other aspects of reproduction. Estrogens appear to regulate these physiological events by binding to the intracellular estrogen receptor (ER). The ligand-bound receptor then interacts with an estrogen response element on DNA and thereby modulates the transcription of specific genes. ER and its mRNA have been detected in brain regions where estrogen plays a central role in the regulation of events essential for procreation (1, 2).Recently, a transgenic mouse was constructed that lacked a functional ER-␣ (3). Initial analysis revealed that ER-␣ knockout (ER␣KO) mice were infertile, failing to show reproductive behavior or a normal estrous cycle (3). Interestingly, in vitro ligand binding studies revealed a 5% residual estrogen binding in the ER␣KO uterus (3), although Western blot analysis was unable to detect ER protein (4). Immunocytochemical studies with the ER␣KO mice were also unable to detect ER immunoreactivity in the brain (5). In spite of these findings, our laboratory has shown that several neurotransmitter and hormone receptor systems, thought to be dependent on estrogen, were not dramatica...

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Ovarian Steroid Regulation of Estrogen and Progesterone Receptor Messenger Ribonucleic Acid in the Anteroventral Periventricular Nucleus of the Rat

Cited by 125 publications

References 70 publications

Progesterone Attenuates Corticotropin-Releasing Factor-Enhanced But Not Fear-Potentiated Startle via the Activity of Its Neuroactive Metabolite, Allopregnanolone

Progesterone Attenuates Corticotropin-Releasing Factor-Enhanced But Not Fear-Potentiated Startle via the Activity of Its Neuroactive Metabolite, Allopregnanolone

Hypothalamic progesterone receptor-A mediates gonadotropin surges, self priming and receptivity in estrogen-primed female mice

Responses in the brain of estrogen receptor α-disrupted mice

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