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Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus
dc.creator | Petrović, Snjezana B | |
dc.creator | Veličković, Nataša | |
dc.creator | Stanojević, Ivana | |
dc.creator | Milosević, Maja S | |
dc.creator | Drakulić, Dunja R | |
dc.creator | Stanojlović, Milos R | |
dc.creator | Horvat, Anica I | |
dc.date.accessioned | 2017-11-23T11:08:03Z | |
dc.date.available | 2015-11-17T10:26:51Z | |
dc.date.issued | 2011 | sr |
dc.identifier.issn | 0306-4522 | sr |
dc.identifier.other | Rad_konverzija_3260 | sr |
dc.identifier.uri | https://radar.ibiss.bg.ac.rs/handle/123456789/1265 | |
dc.description.abstract | Our results, as well as those of others, have indicated that 17 beta-estradiol (E2) exerts its nongenomic effects in neuronal cells by affecting plasma membrane Ca2+ flux. In neuronal cells mitochondria possess Ca2+ buffering properties as they both sequester and release Ca2+. The goal of this study was to examine the rapid non-genomic effect of E2 on mitochondria! Ca2+ transport in hippocampal synaptosomes from ovariectomised rats. In addition, we aimed to determine if, and to what extent, E2 receptors participated in mitochondria! Ca2+ transport modulation by E2 in vitro. E2-specific binding and Ca2+ transport was monitored. At physiological E2 concentrations (0.1-1.5 nmol/L), specific E2 binding to mitochondria isolated from hippocampal synaptosomes was detected with a B-max and K-m of 37.6 +/- 2.6 fmol/mg protein and 0.69 +/- 0.14 nmol/L of free E2, respectively. The main mitochondrial Ca2+ influx mechanism is the Ruthenium Red-sensitive uniporter driven by mitochondrial membrane potential. Despite no effect of E2 on Ca2+ influx, a physiological E2 concentration (0.5 nmol/L) protected mitochondrial membrane potential and consequently Ca2+ influx from the uncoupling agent carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (1 mu mol/L). In neuronal cells the predominant mitochondria! Ca2+ efflux mechanism is the Na+/Ca2+ exchanger. E2 caused Ca2+ efflux inhibition (by 46%) coupled with increased affinity of the Na+/Ca2+ exchanger for Na+. Using E2 receptor (ER alpha and ER beta) antagonists and agonists, we confirmed ER beta's involvement in E2-induced mitochondrial membrane potential protection as well as Ca2+ efflux inhibition. In summary, our results indicate that the nongenomic neuromodulatory role of E2 in rat hippocampus is achieved by affecting mitochondria! Ca2+ transport via, in part, mitochondrial ER beta. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved. | en |
dc.description.sponsorship | Ministry of Sciences and Technological Development of Serbia [173044] | sr |
dc.language.iso | English | sr |
dc.rights | restrictedAccess | |
dc.source | Neuroscience | sr |
dc.title | Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus | en |
dc.type | article | |
dc.rights.license | ARR | |
dcterms.abstract | Милосевић, Маја С; Станојевић, Ивана; Петровић, Сњезана Б; Величковић, Наташа; Станојловић, Милос Р; Хорват, Aница И; Дракулић, Дуња Р; | |
dc.citation.issue | null | sr |
dc.citation.volume | 192 | sr |
dc.citation.epage | 204 | sr |
dc.type.version | publishedVersion | en |
dc.citation.rank | M22 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_1265 |
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