钙通过质膜纳米破裂内流驱动多发性硬化模型中的轴突变性。
Calcium Influx through Plasma-Membrane Nanoruptures Drives Axon Degeneration in a Model of Multiple Sclerosis.
机构信息
Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany; Institute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany.
出版信息
Neuron. 2019 Feb 20;101(4):615-624.e5. doi: 10.1016/j.neuron.2018.12.023. Epub 2019 Jan 24.
Axon loss determines persistent disability in multiple sclerosis patients. Here, we use in vivo calcium imaging in a multiple sclerosis model to show that cytoplasmic calcium levels determine the choice between axon loss and survival. We rule out the endoplasmic reticulum, glutamate excitotoxicity, and the reversal of the sodium-calcium exchanger as sources of intra-axonal calcium accumulation and instead identify nanoscale ruptures of the axonal plasma membrane as the critical path of calcium entry.
轴突损失决定多发性硬化症患者的持续残疾。在这里，我们使用多发性硬化症模型中的体内钙成像来显示细胞质钙水平决定了轴突损失和存活之间的选择。我们排除了内质网、谷氨酸兴奋性毒性和钠钙交换体的反转作为轴内钙积累的来源，而是确定了轴突质膜的纳米级破裂作为钙进入的关键途径。
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