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Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Estrogen and progesterone modulate DA activity in the striatum and nucleus accumbens (NAc) under several conditions [33]. For example, there are estrous cycle-dependent variations in the basal extracellular concentration of striatal DA, in amphetamine (AMPH)-stimulated DA release, and in striatal DA-mediated behaviors. Ovariectomy attenuates basal extracellular DA, AMPH-induced striatal DA release, and behaviors mediated by the striatal DA system. Estrogen rapidly and directly acts on the striatum and NAc via a G protein-coupled membrane estrogen receptor (GPER) to enhance DA release and DA-mediated behaviors. In male rats, estrogen does not affect striatal DA release, and the removal of testicular hormones is also without effect. It has been proposed that estrogen induces rapid changes in neuronal excitability by acting on membrane receptors located in striatal GABAergic neurons and DA terminals. This modulates the dopaminergic terminal excitability, resulting in enhanced DA release.
Radioautographic Localization of Estrogen Receptors in the Rat Uterus: A Tool for the Study of Classical and Nontraditional Mechanisms of Hormone Action
Published in Louis P. Pertschuk, Sin Hang Lee, Localization of Putative Steroid Receptors, 2019
Andrei N. Tchernitchin, Miguel A. Mena, Angel Rodriguez, Mauricio Maturana
Miscellaneous receptors — The affinity spectrum for membrane estrogen receptors is different from that of cytosol-nuclear or eosinophil receptors. While estradiol displays a high affinity for these receptors and estriol has a lower affinity, diethylstilbestrol does not bind (or binds very weakly) to this receptor system.49,50,155 For type II receptors, scarce information is available: nonradioactive estradiol and diethylstilbestrol inhibits binding by type II cytosol receptors; estradiol but not estriol (unless very high doses are used) causes the appearance of type II nuclear receptors; diethylstilbestrol, estradiol, and estriol compete with labeled estradiol for binding to type II nuclear receptors.93,156,157 It is still not clear what responses to estrogen stimulation are mediated by membrane or by type II receptors.
Roles of membrane and nuclear estrogen receptors in spermatogenesis
Published in C. Yan Cheng, Spermatogenesis, 2018
Paul S. Cooke, Manjunatha K. Nanjappa, Sergei G. Tevosian, Rex A. Hess
Expression of ESR1 is predominately cytoplasmic and nuclear. However, approximately 5% of ESR1 localizes to cell membranes.36,37 Although literature describing steroid hormone effects too rapid to be mediated through classical nuclear receptors goes back to the 1950s, for years the identity of these membrane receptors and their mechanism of action remained unknown. A crucial step forward was the demonstration that transfecting a plasmid encoding ESR1 into ESR1-deficient cells led to expression of both nuclear and membrane ESR1.38,39 Furthermore, ESR1 antibodies showed both nuclear and cell membrane staining.39 These findings led to the conclusion that membrane estrogen receptors40 were identical to classical nuclear ESR1.
The role of Gα protein signaling in the membrane estrogen receptor-mediated signaling
Published in Gynecological Endocrinology, 2021
Shuhui Zheng, Lin Wu, Chao Fan, Jingxia Lin, Yaxing Zhang, Tommaso Simoncini, Xiaodong Fu
Estrogens exert rapid, extranuclear effects by their action on the membrane estrogen receptors (mERs). Several mERs have been established. Boonyaratanakornkit et al. [5] have found that the membrane-associated ERα and ERß may occur in the form of homodimers or heterodimers. In addition to the full-length 66 kD ERα, the 46-kD [6] or 36-kD [7] ERα, has been reported at the cell membrane. Besides membrane estrogen receptor α (mERα) and membrane estrogen receptor β (mERβ), other potential mERs have been identified. The most investigated mER among them is G-protein-coupled receptor 30 (GPER or GPR30). GPR30 regulates the rapid transcriptional activation of some genes [8]. Another putative mER, Gq-mER [9] has been described: Gq-mER is found in the arcuate nucleus of the hypothalamus. Gq-mER is believed to play an important role in a variety of homeostasis processes [10]. Besides the mERs mentioned above, other mERs have been reported, such as ER-X and ER x [11,12].
Safety of non-hormonal medications for managing hot flashes
Published in Expert Opinion on Drug Safety, 2022
Pasquale De Franciscis, Maurizio Guida, Antonio Schiattarella, Gaetano Riemma, Nicola Colacurci
Phytoestrogens are the most popular nutraceutical compounds used for menopausal complaints, and its name originates from the Greek word ‘phyto’ (‘plant’) and estrogen. These are nonsteroidal phenolic plant molecules with a chemical estrogen-like structure. The major classes of phytoestrogens are called isoflavones and lignans; major isoflavones include biochanin A, formonentin, genistein, glycitein and daidzein, while enterolactone and enterodiol are the most common lignans. Soybeans represent a natural source of isoflavones, while lignans are found in flaxseed and sesame seed as well as in cereals and vegetables. Despite their natural origin, isoflavones and lignans exert an estrogenic or antiestrogenic effect depending on the circulating estrogen level and intestinal absorption [17]. Phytoestrogens bind both estrogen receptors α (α-ER) and ERβ, but they present a higher affinity toward ERβ receptors even if with less affinity and lower potency than estrogens [18]. The effect of isoflavones is also strictly related to the level of endogenous estradiol because ERs are competitively bound by isoflavones and estradiol [18]. In the case of low levels of endogenous estrogens, the estrogen activity of isoflavones should manifest. In such a scenario, isoflavones are used as a non-MHT related treatment in symptomatic women, especially in long-term administration periods [18]. Moreover, they also show a nongenomic mediated activity throughout the activation of the membrane estrogen receptor α (mERα); therefore, they stimulate several intracellular responses (activation of MAPKs and increased intracellular [Ca2+]). This mechanism is believed to carry out a significant role in tissues that are not considered to be standard targets of estradiol-related actions such as the cardiovascular system and the central nervous system [19]Moreover, they are able to stimulate the synthesis of sex hormone-binding globulin (SHBG) in patients with inherently low SHBG levels [20].