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首页> 外文期刊>The European Journal of Neuroscience >Alpha-synuclein mediates alterations in membrane conductance: a potential role for alpha-synuclein oligomers in cell vulnerability.
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Alpha-synuclein mediates alterations in membrane conductance: a potential role for alpha-synuclein oligomers in cell vulnerability.

机译：α-突触核蛋白介导膜电导的改变：α-突触核蛋白低聚物在细胞脆弱性中的潜在作用。

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摘要

alpha-Synuclein has been linked to the pathogenesis of Parkinson's disease and other synucleinopathies through its propensity to form toxic oligomers. The exact mechanism for oligomeric synuclein-directed cell vulnerability has not been fully elucidated, but one hypothesis portends the formation of synuclein-containing pores within cell membranes leading to leak channel-mediated calcium influx and subsequent cell death. Here we demonstrate synuclein-induced formation of sodium dodecyl sulfate-stable oligomers, intracellular synuclein-positive aggregates, alterations in membrane conductance reminiscent of leak channels and subsequent cytotoxicity in a dopaminergic-like cell line. Furthermore we demonstrate that the synuclein-induced membrane conductance changes are blocked by direct extracellular application of an anti-synuclein antibody. The work presented here confirms that synuclein overexpression leads to membrane conductance changes and demonstrates for the first time through antibody-blocking studies that synuclein plays a direct role in the formation of leak channels.
机译：α-突触核蛋白通过其形成有毒寡聚物的倾向与帕金森氏病和其他突触核蛋白病的发病机理有关。寡聚体针对突触核蛋白定向的细胞脆弱性的确切机制尚未完全阐明，但一种假说预示着细胞膜内含突触核蛋白的孔的形成，导致泄漏通道介导的钙内流并随后导致细胞死亡。在这里，我们证明了突触核蛋白诱导的十二烷基硫酸钠稳定的低聚物，细胞内突触核蛋白阳性聚集体的形成，膜电导的改变让人联想到泄漏通道以及随后在多巴胺能样细胞系中的细胞毒性。此外，我们证明了突触核蛋白诱导的膜电导率变化被抗突触核蛋白抗体的直接细胞外应用所阻断。此处提出的工作证实了突触核蛋白的过度表达会导致膜电导的变化，并首次通过抗体阻断研究证明突触核蛋白在泄漏通道的形成中起着直接作用。

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