Neuroestrogen, rapid action of estradiol, and GnRH neurons

Terasawa, Ei; Kenealy, Brian P.

doi:10.1016/j.yfrne.2012.08.001

Cited by 50 publications

(30 citation statements)

References 162 publications

(240 reference statements)

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“…In the hypothalamus, membrane signaling via ERα is involved in gonadotropin secretion [100] and sexual behavior [101], where it appears to play a vital modulatory role. The modulation of these hypothalamic homeostatic functions by E 2 is due in large part to the attenuation of the coupling of metabotropic G i/o coupled receptors and their effector systems [102,103].…”

Section: Pathophysiological Implications Of Membrane Signalingmentioning

confidence: 99%

Rapid steroid hormone actions via membrane receptors

Schwartz

Verma

Bivens

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Steroid hormones regulate a wide variety of physiological and developmental functions. Traditional steroid hormone signaling acts through nuclear and cytosolic receptors, altering gene transcription and subsequently regulating cellular activity. This is particularly important in hormonally-responsive cancers, where therapies that target classical steroid hormone receptors have become clinical staples in the treatment and management of disease. Much progress has been made in the last decade in detecting novel receptors and elucidating their mechanisms, particularly their rapid signaling effects and subsequent impact on tumorigenesis. Many of these receptors are membrane-bound and lack DNA-binding sites, functionally separating them from their classical cytosolic receptor counterparts. Membrane-bound receptors have been implicated in a number of pathways that disrupt the cell cycle and impact tumorigenesis. Among these are pathways that involve phospholipase D, phospholipase C, and phosphoinositide-3 kinase. The crosstalk between these pathways has been shown to affect apoptosis and proliferation in cardiac cells, osteoblasts, and chondrocytes as well as cancer cells. This review focuses on rapid signaling by 17β-estradiol and 1α,25-dihydroxy vitamin D3 to examine the integrated actions of classical and rapid steroid signaling pathways both in contrast to each other and in concert with other rapid signaling pathways. This new approach lends insight into rapid signaling by steroid hormones and its potential for use in targeted drug therapies that maximize the benefits of traditional steroid hormone-directed therapies while mitigating their less desirable effects.

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Section: Pathophysiological Implications Of Membrane Signalingmentioning

confidence: 99%

Rapid steroid hormone actions via membrane receptors

Schwartz

Verma

Bivens

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Indeed, they have shown that rising estradiol levels initiate a membrane-associated estradiol signaling cascade involving the transactivation of metabotropic glutamate receptor type 1a (mGluR1a) in hypothalamic astrocytes, which ultimately leads to the synthesis of progesterone, critical for initiating the LH surge. Moreover, primate studies have identified rapid excitatory effects of estradiol on GnRH neuronal activity and suggest that estradiol locally synthesized in the hypothalamus may play a significant role in the control of the preovulatory surge and/or pulsatile release of GnRH [96]. Since data from rodents and humans suggest that astrocytes are a source of estrogens in the brain [97,98], these observations raise the possibility that astrocytes could contribute to the regulation of GnRH neuronal activity and secretion via the local synthesis of neuroestrogens.…”

Section: Glial Cells: Sensors and Effectors Of Sex Steroid Actions Inmentioning

confidence: 99%

“…Importantly, clear differences have been described in the neural and hormonal control of the preovulatory GnRH/LH surge between rodents and higher primates [96,105]. In addition, astrocytes in the human cerebral cortex exhibit increased size, structural complexity, diversity and speed of Ca 2+ wave propagation than their rodent counterparts [106].…”

Section: Do Glial Cells Regulate the Gnrh System In The Human Brain?mentioning

confidence: 99%

Role of Glia in the Regulation of Gonadotropin-Releasing Hormone Neuronal Activity and Secretion

Sharif

Baroncini

Prévot³

2013

Neuroendocrinology

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Gonadotropin-releasing hormone (GnRH) neurons are the final common pathway for the central control of reproduction. The coordinated and timely activation of these hypothalamic neurons, which determines sexual development and adult reproductive function, lies under the tight control of a complex array of excitatory and inhibitory transsynaptic inputs. In addition, research conducted over the past 20 years has unveiled the major contribution of glial cells to the control of GnRH neurons. Glia use a variety of molecular and cellular strategies to modulate GnRH neuronal function both at the level of their cell bodies and at their nerve terminals. These mechanisms include the secretion of bioactive molecules that exert paracrine effects on GnRH neurons, juxtacrine interactions between glial cells and GnRH neurons via adhesive molecules and the morphological plasticity of the glial coverage of GnRH neurons. It now appears that glial cells are integral components, along with upstream neuronal networks, of the central control of GnRH neuronal function. This review attempts to summarize our current knowledge of the mechanisms used by glial cells to control GnRH neuronal activity and secretion.

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“…42). In fact, we and others have shown that the involvement of non-ER␣ membrane receptors, such as GPR30, STX-sensitive receptors, and ER␤, is important for rapid signaling in GnRH neurons (12,13,(43)(44)(45). Moreover, experiments using rat S-ME fragments show that activation of Figure 5.…”

Section: Discussionmentioning

confidence: 95%

Prolonged Infusion of Estradiol Benzoate Into the Stalk Median Eminence Stimulates Release of GnRH and Kisspeptin in Ovariectomized Female Rhesus Macaques

et al. 2015

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Our recent study indicates that a brief infusion (20 min) of estradiol (E2) benzoate (EB) into the stalk-median eminence (S-ME) stimulates GnRH release with a latency of approximately 10 minutes. In contrast to the effect induced by a brief infusion of EB, it has previously been shown that systemic EB administration suppresses release of GnRH, kisspeptin, and LH with a latency of several hours, which is known as the negative feedback action of E2. We speculated that the differential results by these 2 modes of EB administration are due to the length of E2 exposure. Therefore, in the present study, the effects of EB infusion for periods of 20 minutes, 4 hours, or 7 hours into the S-ME of ovariectomized female monkeys on the release of GnRH and kisspeptin were examined using a microdialysis method. To assess the effects of the EB infusion on LH release, serum samples were also collected. The results show that similar to the results with 20-minute infusion, both 4- and 7-hour infusions of EB consistently stimulated release of GnRH and kisspeptin from the S-ME accompanied by LH release in the general circulation. In contrast, sc injection of EB suppressed all 3 hormones (GnRH, kisspeptin, and LH) measured. It is concluded that regardless of the exposure period, direct E2 action on GnRH and kisspeptin neurons in the S-ME, where their neuroterminals are present, is stimulatory, and the E2-negative feedback effects do not occur at the S-ME level.

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Neuroestrogen, rapid action of estradiol, and GnRH neurons

Cited by 50 publications

References 162 publications

Rapid steroid hormone actions via membrane receptors

Rapid steroid hormone actions via membrane receptors

Role of Glia in the Regulation of Gonadotropin-Releasing Hormone Neuronal Activity and Secretion

Prolonged Infusion of Estradiol Benzoate Into the Stalk Median Eminence Stimulates Release of GnRH and Kisspeptin in Ovariectomized Female Rhesus Macaques

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