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Paech K, Webb P, Kuiper GGJM, Nilsson S, Gustafsson J, Kushner PJ, Scanlan TS: Differential ligand activation of estrogen receptors ERα and ERβ at AP1 sites. Science 1997, 277:1508-1510. Estrogens can regulate gene expression either through a classical estrogen response element or from an AP-1 enhancer in combination with the AP-1 transcription factors, Fos and Jun. This study used HeLa cells transfected with either ER-α or ER-β to show differential 17β-estradiol- induced transcriptional activation from the AP-1 site: with ER-α, estradiol promoted transcription, whereas with ER-β, estradiol inhibited transcription. These results imply that ER-α and ER-β can play different roles in gene regulation.
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Paech, K.1
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Differential response of estrogen receptor alpha and estrogen receptor beta to partial estrogen agonists/antagonists
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Barkhem T, Carlsson B, Nilsson Y, Enmark E, Gustafsson J, Nilsson S: Differential response of estrogen receptor alpha and estrogen receptor beta to partial estrogen agonists/antagonists. Mol Pharmacol 1998, 54:105-112. The pharmacology of genomic ERs is complicated. This study defines the relative potencies of various agonists and antagonists at ER-α versus ER-β, and shows that significant differences in ligand potency exist between the two receptors. This type of information will be key in the development of pharmaceutical agents with selective action at one or another ER.
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Barkhem, T.1
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Oterlund M, Kuiper GG, Gustafsson J, Hurd YL: Differential distribution and regulation of estrogen receptor-alpha and -beta mRNA within the female rat brain. Mol Brain Res 1998, 54:175-180. Estrogens regulate ER expression in multiple brain areas. This study demonstrates differential feedback regulation of ER-α and ER-β in various regions of the hypothalamus and amygdala. The data provide a basis for the opposite effects of estradiol in regulating estrogen-sensitive functions mediated by different brain nuclei.
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Shughrue PJ, Scrimo PJ, Merchenthaler I: Evidence for the colocalization of estrogen receptor beta mRNA and estrogen receptor alpha immunoreactivity in neurons of the rat forebrain. Endocrinology 1998, 139:5267-5270. The ability of ER-α and ER-β to form heterodimers potentially adds a new level of complexity to estrogen regulation of gene expression. However, such heterodimerization is only relevant if the two ERs are expressed in the same cells. This study suggests co-expression of ER-β mRNA and ER-α protein in some brain areas, but not in others. Although definitive proof of co-expression will require detection of both proteins in individual cells, this study represents an intriguing initial step toward that goal.
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Endocrinology
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Shughrue, P.J.1
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The complete primary structure of human estrogen receptor beta (hER beta) and its heterodimerization with ER alpha in vivo and in vitro
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Ogawa S, Inoue S, Watanabe T, Hiroi H, Orimo A, Hosoi T, Ouchi Y, Muramatsu M: The complete primary structure of human estrogen receptor beta (hER beta) and its heterodimerization with ER alpha in vivo and in vitro. Biochem Biophys Res Commun 1998, 243:122-126.
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Petersen DN, Tkalcevic GT, Koza-Taylor PH, Turi TG, Brown TA: Identification of estrogen receptor beta2, a functional variant of estrogen receptor beta expressed in normal rat tissues. Endocrinology 1998, 139:1082-1092.
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Maruyama K, Endoh H, Sasaki-Iwaoka H, Kanou H, Shimaya E, Hashimoto S, Kato S, Kawashima H: A novel isoform of rat estrogen receptor beta with 18 amino acid insertion in the ligand binding domain as a putative dominant negative regulator of estrogen action. Biochem Biophys Res Commun 1998, 246:142-147.
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Moore JT, McKee DD, Slentz-Kesler K, Moore LB, Jones SA, Horne EL, Su JL, Kliewer SA, Lehmann JM, Willson TM: Cloning and characterization of human estrogen receptor beta isoforms. Biochem Biophys Res Commun 1998, 247:75-78.
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Gu Q, Moss RL: Novel mechanism for non-genomic action of 17β estradiol on kainate-induced currents in isolated rat CA1 hippocampal neurons. J Physiol 1998, 506.3:745-754. The mechanism by which estrogen can rapidly alter neuronal excitability is unknown. This study provides key insight into estrogen's nongenomic actions by using bovine serum albumin coupled estradiol to show that estradiol needs to be present on both sides of the membrane to potentiate kainate-evoked currents in hippocampal CA1 pyramidal cells.
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Woolley CS, McEwen BS: Estradiol mediates fluctuation in hippocampal synapse density during the estrous cycle in the adult rat. J Neurosci 1992, 12:2549-2554.
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Woolley CS, Weiland NG, McEwen BS, Schwartzkroin PA: Estradiol increases the sensitivity of hippocampal CA1 pyramidal cells to NMDA receptor-mediated synaptic input: Correlation with dendritic spine density. J Neurosci 1997, 17:1848-1859. Although estradiol has been shown to alter the structural connectivity of adult neurons, the electrophysiological consequences of the structural changes are unclear. We performed a cell-by-cell comparison of hippocampal CA1 pyramidal cell sensitivity to synaptic input and dendritic spine density by recording individual neurons and then filling the cells with biocytin to visualize dendritic spines following recording. Cells in slices from both ovariectomized, estradiol-treated and control ovariectomized animals were recorded. It was found that estradiol induced greater sensitivity to NMDA-, but not nonNMDA-, receptor-mediated input and that increased sensitivity to NMDA-receptor-mediated input is statistically correlated with a greater density of dendritic spines. These data suggest that new spine synapses induced by estrogen may contain primarily NMDA receptors.
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He Y, Janssen WG, Morrison JH: Synaptic coexistence of AMPA and NMDA receptors in the rat hippocampus: A postembedding immunogold study. J Neurosci Res 1998, 54:444-449. Although synapses containing only the NMDA subtype of ionotropic glutamate receptor have been hypothesized based on electrophysiological data from immature hippocampal tissue, their existence in the adult brain is highly controversial. This study used electron microscopic immunogold double and triple (with GABA) labeling to demonstrate a population of synapses that contain NR1 (the obligatory subunit of the NMDA receptor) but not GluR2 (a subunit of the AMPA receptor), suggesting that synapses with only NMDA receptors may exist in the adult hippocampus.
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Murphy DD, Segal M: Regulation of dendritic spine density in cultured rat hippocampal neurons by steroid hormones. J Neurosci 1996, 16:4059-4068.
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Murphy DD, Cole NB, Greenberger V, Segal M: Estradiol increases dendritic spine density by reducing GABA neurotransmission in hippocampal neurons. J Neurosci 1998, 18:2550-2559. Hippocampal interneurons contain ER-α, which suggests that these cells may be a primary site of estrogen action to induce new dendritic spines on pyramidal cells. This study directly confirms this hypothesis in cultured hippocampal neurons by showing that estradiol treatment reduces expression of both GABA and GAD (glutamic acid decarboxylase), and that treatment of cultures with mercaptopropionic acid (MA), an inhibitor of GABA synthesis, mimics the effect of estradiol on spine density. Importantly, the effects of MA and estradiol are not additive, suggesting that they share a common mechanism.
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Murphy, D.D.1
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Murphy DD, Cole NB, Segal M: Brain-derived neurotrophic factor mediates estradiol-induced dendritic spine formation in hippocampal neurons. Proc Natl Acad Sci USA 1998, 95:11412-11417. Estradiol treatment of hippocampal cultures decreases levels of BDNF. To demonstrate the role of BDNF in regulating spine density, the authors show that exogenous BDNF can block the estradiol-induced increase in dendritic spine density, whereas BDNF depletion with a selective anti-sense oligonucleotide or addition of function-blocking BDNF antibodies mimics the effect of estradiol.
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Gibbs RB: Levels of trKA and BDNF mRNA, but not NGF mRNA, fluctuate across the estrous cycle and increase in response to acute hormone replacement. Brain Res 1998, 787:259-268. This study shows that ovarian steroid hormones regulate BDNF mRNA levels in the hippocampus in vivo. Results from estrous cycle studies show that BDNF mRNA levels are lowest when estradiol and progesterone are high. Hormone treatment experiments, however, indicate that estradiol in combination with progesterone increases BDNF mRNA levels. Thus, the precise roles that estradiol and progesterone play in regulating BDNF are currently unresolved. Nevertheless, it is clear that BDNF is regulated by estradiol and progesterone, and thus may be involved in regulating dendritic spine density in vivo.
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