Oestrogen Receptor β: Role in Neurohypophyseal Neurones

Sladek, Celia D.; Somponpun, Suwit J.

doi:10.1111/j.0953-8194.2004.01187.x

Cited by 17 publications

(17 citation statements)

References 66 publications

(93 reference statements)

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“…This is in accordance with numerous observations showing that estrogens enhance OT secretion by modulating the electrical activity of OT neurons (35), increasing OT gene expression (13) and central and peripheral release (95,96). However, some caution is necessary in interpreting our results, because reports of gonadal steroid effects on magnocellular neurons are conflicting (74). Indeed, the site of action of the steroid in OT neurons has not been identified, and we still do not know whether its effect is direct or indirect.…”

Section: Ot Induces Morphological Plasticitysupporting

confidence: 92%

“…Long-term genomic effects are mediated by nuclear estrogen receptors, ER␣ or ER␤ (46,73). Rat OT neurons lack the former (73,74) and Ͻ10% express the latter (75). In view of the rapidity of the effects of the steroid on the anatomy of the SON (43), it is more probable that estrogens act via a plasmalemmal mechanism (65), mobilizing intracellular calcium and inducing signaling cascades that result in activation of gene expression and ultimately synapse formation.…”

Section: Ot Induces Morphological Plasticitymentioning

confidence: 99%

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Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Theodosis¹,

Trailin²,

Poulain³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Theodosis, Dionysia T., Andrei Trailin, and Dominique A. Poulain. Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus. Am J Physiol Regul Integr Comp Physiol 290: R1175-R1182, 2006; doi:10.1152/ajpregu.00755.2005.-Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany astrocytic transformations so that an increased number of synapses are associated with reduced astrocytic coverage of postsynaptic elements, whereas synaptic numbers are reduced on reestablishment of glial coverage. A system that exemplifies activity-dependent structural synaptic plasticity in the adult brain is the hypothalamo-neurohypophysial system, and in particular, its oxytocin component. Under strong, prolonged activation (parturition, lactation, chronic dehydration), extensive portions of somatic and dendritic surfaces of magnocellular oxytocin neurons are freed of intervening astrocytic processes and become directly juxtaposed. Concurrently, they are contacted by an increased number of inhibitory and excitatory synapses. Once stimulation is over, astrocytic processes again cover oxytocinergic surfaces and synaptic numbers return to baseline levels. Such observations indicate that glial ensheathment of neurons is of consequence to neuronal function, not only directly, for example by modifying synaptic transmission, but indirectly as well, by preparing neuronal surfaces for synapse turnover.NEURONS, GLIA, AND SYNAPTIC inputs are not static elements because they undergo dynamic transformations. This can take place under normal physiological conditions and highlights the adult nervous system's remarkable capacity to undergo restructuring to meet particular functional requirements. A change in the morphology of neurons, and especially of afferent inputs controlling their activity, can have important consequences on their respective functions. These modifications are often accompanied by remodeling of adjacent glia, which has further impact on neuronal activity by modifying the immediate extracellular microenvironment, thereby influencing synaptic and volume transmission.The hypothalamo-neurohypophysial system (HNS), and in particular, its oxytocinergic component, is a familiar model for this kind of morphological neuronal and glial plasticity (57,76). Oxytocin (OT) neurons accumulate in well-defined regions in the hypothalamus, the supraoptic (SON), and paraventricular (PVN) nuclei, and release OT mainly from axon terminals in the neurohypophysis to act as a neurohormone in vital functions like parturition, lactation, and osmotic regulation. Critical for this systemic secretion is the concomitant exocytotic release of the peptide from somata and dendrites of OT neurons themselves in the SON and PVN. This central release facilitates the synchronous high-frequency activity of...

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Section: Ot Induces Morphological Plasticitysupporting

confidence: 92%

Section: Ot Induces Morphological Plasticitymentioning

confidence: 99%

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Theodosis¹,

Trailin²,

Poulain³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Evidence also suggests a role for the ER-b, as this receptor is expressed in magnocellular vasopressin neurons in the PVN and SON. [34][35][36] Finally, it is well established that progesterone plays an important role in the hypothalamic regulation of oxytocin via the progesterone metabolite, allopregnanalone, and the progesterone receptor is not expressed in this region. 37 An interesting study also linked allopregnanalone to nitric oxide production and plasma volume expansion.…”

Section: 30mentioning

confidence: 99%

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Stachenfeld

2014

Reprod. Sci.

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Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because during this period women can retain water at an accelerated pace and much faster than they do sodium. This review proposes that estrogen and progestogen exposure play an important role in the increased risk of hyponatremia in menopausal women. Estrogen and progesterone exposure have important effects on both body fluid regulation and cardiovascular function and both of these reproductive hormones impact blood pressure responses to sodium loads. This article provides information on the effects of female reproductive hormones and hormone therapy (HT) on fluid regulation and cardiovascular function during menopause. Thirst-and fluid-regulating hormones respond to both osmotic and volume stimuli. Aging women maintain thirst sensitivity to osmotic stimuli but lose some thirst sensitivity to changes in central body fluid volume. Thus, older adults are more at risk of dehydration because they may replenish fluids at a slower rate. Estrogen therapy increases osmotic sensitivity for mechanisms to retain body water so may help menopausal women control body fluids and avoid dehydration. Some progestogens can mitigate estradiol effects on water and sodium retention through competition with aldosterone for the mineralocorticoid receptor and attenuating aldosterone-mediated sodium retention in the distal tubule. However, some progestogens can increase cardiovascular risks. Appropriate balance of these hormones within HT is important to avoid the negative consequences of body fluid and sodium retention, including edema and hypertension.Keywords hormone therapy, estrogen, progesterone, body fluid regulation, arginine vasopressin Reproductive surgeries leave women more susceptible to postoperative hypervolemic hyponatremia because women retain water at a faster rate than sodium during this period, 1-5 especially after reproductive surgeries. 4,7 Indeed, women are at high risk of postoperative hyponatremia even after relatively low-risk surgeries such as operative hysteroscopy. In such surgeries, glycine solution (lacking electrolytes) is used as a distension medium and can cause intravascular volume retention, increasing the risk of hyponatremia, cerebral and/or pulmonary edema, psychological disturbances, and even death. 4,[8][9] A combination of anesthesia, nausea, and the postsurgical experience tends to increase arginine vasopressin (AVP). This hormone, the primary hormone involved in free water retention, is also associated with altered astroglia volume regulation in both pre-and postmenopausal (PM) women. 3,5,10,11 Studies in animals support an important role for estradiol in increasing astroglia volume in women with hyponatremia, suggesting a role for female reproductive hormones in the dire consequences that can be associated with postoperative hyponatremia in both young and PM women. 6,12 Hormones During MenopauseThe stages of the menopause transition are classified by changes in menstrual bleeding, concomitant...

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“…ER␣ is expressed in the breast, uterus, and bone, while ER␤ is expressed predominantly in the prostate, central nervous system, and intestinal tissues (23,24,31,50,62). Even within a single tissue, the expression pattern of each subtype is cell type specific.…”

mentioning

confidence: 99%

Coactivation of Estrogen Receptor β by Gonadotropin-Induced Cofactor GIOT-4

Kouzu-Fujita

Mezaki

Sawatsubashi

et al. 2009

Molecular and Cellular Biology

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Estrogen exerts its diverse effects through two subtypes of estrogen receptors (ER), ER␣ and ER␤. Each subtype has its own distinct function and expression pattern in its target tissues. Little, however, is known about the transcriptional regulatory mechanism of ER␤ in the major ER␤-expressing tissues. Using biochemical methods, we identified and described a novel ER␤ coactivator. This protein, designated GIOT-4, was biochemically purified from 293F cells. It coactivated ER␤ in ovarian granulosa cells. GIOT-4 expression was induced by stimulation with follicle-stimulating hormone (FSH). GIOT-4 recruited an SWI/SNF-type complex in a ligand-independent manner to ER␤ as an ER subtype-specific physical bridging factor and induced subsequent histone modifications in the ER␤ target gene promoters in a human ovarian granulosa cell line (KGN). Indeed, two ER␤-specific target genes were upregulated by FSH at a specific stage of a normal ovulatory cycle in intact mice. These findings imply the presence of a novel regulatory convergence between the gonadotropin signaling cascade and ER␤-mediated transcription in the ovary.Estrogen plays important roles in many target organs, including the female reproductive organs, the central nervous system, and bone. Estrogen exerts its diverse biological actions through binding to and activating one of two nuclear estrogen receptor (ER) subtypes (ER␣ or ER␤) (12,22,35,40). ERs are members of the nuclear receptor (NR) gene superfamily. ERs, bound to and activated by estrogen, bind to specific DNA sequences called estrogen-responsive elements (ERE) to induce target genes (14,21).Like the other NR members, the ER requires the cooperation of distinct classes of coregulators and multiprotein coregulator complexes in order to initiate estrogen-mediated chromatin reorganization (16,46). These complexes appear to modify the chromatin configuration in a highly regulated manner by controlling nucleosomal rearrangement and enzymecatalyzed modifications of histone tails. By altering chromatin structure, the coregulator complexes facilitate bridging between NRs and basal transcription factors, along with RNA polymerase II, thereby controlling transcription. As for the nucleosomal rearrangement, two major classes of chromatinmodifying complexes that coregulate NRs have been well-characterized. One class is the histone-modifying complexes, including discrete subfamilies of transcription coregulatory complexes (2,29,36). The best-characterized NR coregulator complexes possess either histone acetylase or histone deacetylase activities. Recently, histone methylases/demethylases have also been shown to be significant NR coregulators. The other class of coregulator complexes is ATP-dependent chromatinremodeling complexes. These complexes use ATP hydrolysis to rearrange nucleosomal arrays in a noncovalent manner to facilitate or prevent the access of NRs to nucleosomal DNA (5,17,33). These ATP-dependent chromatin-remodeling complexes have been classified into three subfamilies based on the major catalytic ...

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Oestrogen Receptor β: Role in Neurohypophyseal Neurones

Cited by 17 publications

References 66 publications

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Hormonal Changes During Menopause and the Impact on Fluid Regulation

Coactivation of Estrogen Receptor β by Gonadotropin-Induced Cofactor GIOT-4

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