Regulation of Estrogen Receptor Concentrations in the Rat Brain: Effects of Sustained Androgen and Estrogen Exposure

Brown, Theodore J.; Scherz, Bernadette; Hochberg, Richard B.; MacLusky, Neil J.

doi:10.1159/000126935

Cited by 87 publications

(51 citation statements)

References 17 publications

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“…In female rats, estradiol treatment downregulated estrogen receptor binding in the hypothalamus and amygdala [3, 4]. Long-term (3 months) ovariectomy in rats downregulated brain ER-β but did not alter abundance of ER-α [21].…”

Section: Discussionmentioning

confidence: 99%

“…Estradiol downregulated ER-α in the hypothalamus statistically significantly at the protein level and almost statistically significantly at the mRNA level. The downregulation of this receptor in the fetal hypothalamus is reminiscent of the downregulation of ER in hypothalamic nuclei in adult rats exposed to large doses of estradiol [3, 4]. In contrast to the effect in the hypothalamus, estradiol increased ER-α in the hippocampus (at the mRNA level) and cerebellum (at the protein level).…”

Section: Discussionmentioning

confidence: 99%

“…The effect of increases in circulating estradiol concentrations on the abundance of estrogen receptor forms in the fetal brain is unknown. Specifically, it is not known whether receptor abundance is downregulated in response to estrogen as it is in the mammary gland, brain, and pituitary in adult rats and mice [2,3,4,5]. If so, it is possible that the influence of estrogen on receptor abundance is specific to different brain regions, and it is possible that the regulation of the receptor is different in the fetus compared to the adult.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral Hypoperfusion Increases Estrogen Receptor Abundance in the Ovine Fetal Brain and Pituitary

Wood¹

2007

Neuroendocrinology

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Background/Aims: Estrogen is an important component of fetal neuroendocrine function in late-gestation fetal sheep; however, little is known about the regulation of estrogen receptor abundance in the brain and pituitary of fetuses. The present study was performed to test the hypotheses that estrogen receptor abundance in the fetal brain and pituitary are influenced by circulating estradiol concentrations and that they are acutely regulated after cerebral hypoperfusion. Methods: We studied 16 time-dated fetal sheep (124–128 days gestation) that were chronically catheterized and instrumented at least 5 days before study. Four groups (n = 4 each) were studied in which fetuses received estradiol (0.25 mg/day, producing physiological increases in fetal plasma estradiol concentrations) or placebo implants, and in which fetuses received a 10-min period of brachiocephalic occlusion (BCO) or sham-BCO. One hour after BCO or sham-BCO, fetuses were euthanized and tissues rapidly removed for analysis of estrogen receptors (ER)-α and -β at the mRNA and protein levels. Results: Both BCO and estradiol treatment were effective in changing ER expression, although the effects were region-specific. BCO dramatically increased ER-α in the pituitary and both ER-α and ER-β in the brainstem, while decreasing ER-α expression in the hypothalamus. Estradiol treatment decreased ER-α expression in the hypothalamus, whereas it increased ER-α expression in the brainstem, cerebral cortex and hippocampus. Conclusions: We conclude that the expression of ER-α and ER-β in the brain and pituitary of fetal sheep are influenced by circulating estrogen concentrations and acutely regulated in response to cerebral hypoperfusion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cerebral Hypoperfusion Increases Estrogen Receptor Abundance in the Ovine Fetal Brain and Pituitary

Wood¹

2007

Neuroendocrinology

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“…In the current study, acute EB replacement also reduced ER␣-ir in SGN of OVX females. Although a classic negative feedback to ER␣-ir in the brain has been demonstrated with sustained E exposure using capsule or daily injection (22,23), this report is unique in its demonstration of the acute modulatory effect of E on ER␣-ir, suggesting the sensitivity of SGN to E. It has been suggested that the reduction of ER␣-ir can be a result of ligand-induced immunoreactivity loss, if a specific antibody is used directly against the ligand binding domain of ER␣ (24). However, we have reduced the chance of this mechanism by careful selecting an antibody directed against the amino acids 580-599, an epitope in F domain near the C-terminals of the ER␣.…”

Section: Discussionmentioning

confidence: 99%

A recently identified hypothalamic nucleus expressing estrogen receptor α

Mori¹,

Matsuda²,

Pfaff³

et al. 2008

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

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We report evidence for the existence of a unique nucleus in the rat hypothalamus. This nerve cell group is situated in the interstitial area between the arcuate nucleus and ventromedial nucleus of the hypothalamus, and is primarily oriented sagittally, in a spindle shape. This nucleus was a well defined structure in Nissl-stained sections because of its location in an otherwise cell-poor zone. This sagittalis nucleus of the hypothalamus (SGN) exhibits significant sex differences in its volume and cell numbers, as defined by Nissl staining and estrogen receptor (ER) ␣ immunoreactivity (ir), being significantly larger in males than in females. Treatment of neonatal females with testosterone eliminated these sex differences. It is noteworthy that adult female rats have estrous cycle-related variations in the ER␣-ir cell distribution, decreasing during the proestrus phase of the cycle. Pharmacological experiments demonstrated that the single injection of estradiol benzoate had a significant effect on the ER␣-ir cell count, suggesting the hormonal responsiveness of SGN neurons. This unique hypothalamic nucleus with its morphological sex differences and hormonal responsiveness is embedded in a region important for the regulation of endocrine functions and sexual behaviors.sexual difference ͉ estrous cycle ͉ calbindinD-28k ͉ sagittalis nucleus A fter the comprehensive neuroanatomical charting of neurons expressing mRNAs for estrogen receptors (1) and subsequent estradiol binding (2), it was assumed that the understanding of the neuroanatomy of estrogen action in the brain was fairly complete. Here, however, we have discerned a hitherto unrecognized cell group that expresses estrogen receptor (ER) ␣ and exhibits sex differences.A number of important sex differences have already been described in the mammalian brain (3, 4). Most of these are organized by the action of the gonadal steroids in the critical period: during the few days before to after birth in rodents (4). In this period, an elevated amount of testosterone (T) is secreted from the male fetal testes and converted to estradiol (E) by the enzyme aromatase in the hypothalamus. Formation of E causes permanent masculinization of the brain (5). This masculinization is also experimentally induced in females by the administration of E in the critical period (3, 6). These morphological sex differences in the brain are likely among the neuroanatomical mechanisms for the physiological sex differences in adult brain function (7,8).At the age of puberty, the functional sex-related differences begin to appear, indicated by a sudden rise in the secretion of gonadotrophic hormones: luteinizing hormone (LH) and follicle-stimulating hormone, followed by an increase in gonadal steroids (9). The gonadal steroids, particularly E, orchestrate the neuroendocrine circuits that coordinate sex-specific behaviors. This E signaling is importantly mediated by ERs (3), which are in fact abundant in the sexual dimorphic nuclei in the hypothalamus, such as the anteroventral periventricular ...

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“…Potential factors that need to be considered include catecholamines, thyrotrophin-releasing hormone, GABA, and serotonin [13, 16, 21, 25]. In addition, androgen and estrogen receptors are distributed in a gender-specific manner especially within the hypothalamus and brainstem regions associated with thermoregulation and control of breathing [31, 32, 33, 34, 35]. …”

Section: Discussionmentioning

confidence: 99%

Gender Comparisons of Control of Breathing and Metabolism in Conscious Mice Exposed to Cold

Schlenker

Hansen²,

Pfaff³

2002

Neuroendocrinology

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We evaluated the effects of 2 h of warm (24°C) and cold (6°C) exposure on metabolism and ventilation (v̇_E) in conscious male and female Harlan ICR Swiss Webster mice exposed to air, and 8% O₂ in N₂ (hypoxia) and to 5% CO₂ in O₂ (hypercapnia) for 2 min each at both temperatures. All cold-exposed mice increased O₂ consumption (v̇_O2), and maintained body temperature. Cold-exposed females doubled their tidal volume, increased their v̇_E fivefold, and doubled their ventilatory equivalent to v̇_O2 (v̇_E/v̇_O2). In contrast, cold-exposed males decreased tidal volume and doubled v̇_E relative to warm exposure. The ventilatory equivalent of males was similar during warm and cold exposure. During warm exposure, mice of both genders increased their ventilatory responses to both hypoxia and to hypercapnia by different mechanisms. In contrast, during cold exposure, these responses were blunted relative to air measurements in females and decreased below air values in males. Thus, cold exposure was able to elicit gender-specific ventilatory and metabolic responses.

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Regulation of Estrogen Receptor Concentrations in the Rat Brain: Effects of Sustained Androgen and Estrogen Exposure

Cited by 87 publications

References 17 publications

Cerebral Hypoperfusion Increases Estrogen Receptor Abundance in the Ovine Fetal Brain and Pituitary

Cerebral Hypoperfusion Increases Estrogen Receptor Abundance in the Ovine Fetal Brain and Pituitary

A recently identified hypothalamic nucleus expressing estrogen receptor α

Gender Comparisons of Control of Breathing and Metabolism in Conscious Mice Exposed to Cold

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