摘要
在目前研究中我们建立一个模型(通过暴露在一个低浓度淀粉样β(25-35)肽(Aβ,2μM)的器官型海马体培养物中而造成的慢性神经损伤)来分析17-β雌二醇(17β-E2,10nM)的时间相关影响。神经元死亡于7天后出现,在前24小时或一起或暴露在Aβ后48小时添加17β-E2可以防止神经元死亡。这个影响是效仿选择性雌激素受体激动剂αPPT(100nM)的。Aβ的治疗导致前突触蛋白和后突触蛋白突触素和PSD95的早期和暂时(16-72h)上升,然后在神经元死亡时(7天)下降,17β-E2可以阻止全过程。在暴露于Aβ中72小时后,突触活性提高(谷氨酸盐含量上升,加快装填和卸载FM1-43-标记的突触小囊泡)。这些影响全被能被17-β-E2阻止。这些数据指出雌激素对早期Aβ-引发的突触损伤的有益作用。
关键词: 17-β雌二醇,阿尔茨海默病,雌激素受体α,突触多动,突触素
Current Alzheimer Research
Title:Early β-Amyloid-induced Synaptic Dysfunction Is Counteracted by Estrogen in Organotypic Hippocampal Cultures
Volume: 13 Issue: 6
Author(s): Sara Merlo, Simona Federica Spampinato, Francisco Capani, Maria Angela Sortino
Affiliation:
关键词: 17-β雌二醇,阿尔茨海默病,雌激素受体α,突触多动,突触素
摘要: In the present study we set up a model of slow progression of neuronal injury by exposing organotypic hippocampal cultures to a low concentration of Amyloid β (25-35) peptide (Aβ, 2 μM) to analyze the time-related effects of 17-β estradiol (17β-E2, 10 nM). Neuronal death occurs after 7 d and is prevented by addition of 17β-E2 24 h prior to, together with or 48 h after exposure to Aβ. This effect is mimicked by selective ERα agonist PPT (100 nM). Treatment with Aβ leads to early and transient (16-72 h) increase of pre- and post-synaptic proteins synaptophysin and PSD95, followed by a decrease coincident with neuronal death (7d), all prevented by 17β-E2. At 72 h of Aβ exposure, synaptic activity is increased, as by higher levels of glutamate and increased loading and unloading of FM 1-43-labeled synaptic vesicles. All these effects are also prevented by 17β-E2. These data point out beneficial effects of estrogen on early Aβ-induced synaptic disruption.
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Cite this article as:
Sara Merlo, Simona Federica Spampinato, Francisco Capani, Maria Angela Sortino , Early β-Amyloid-induced Synaptic Dysfunction Is Counteracted by Estrogen in Organotypic Hippocampal Cultures, Current Alzheimer Research 2016; 13 (6) . https://dx.doi.org/10.2174/1567205013666160125113509
DOI https://dx.doi.org/10.2174/1567205013666160125113509 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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