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人抗nr1自身抗体诱导突触病理与突触后NMDA受体的功能相关丧失

Biophotonics Congress: Optics in the Life Sciences Congress 2019 (BODA,BRAIN,NTM,OMA,OMP) Pub Date : 2019-04-14 DOI:10.1364/boda.2019.jt4a.12
L. Schmidl, Luise Röpke, M. Ceanga, J. Kreye, N. K. Wenke, H. Haselmann, H. Prüss, C. Geis
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引用次数: 0

摘要

我们利用LSM和超分辨率显微镜研究了抗n -甲基- d -天冬氨酸受体(NMDAR)抗体在神经元和自身免疫性脑炎小鼠模型中的致病作用。我们发现突触NMDARs的功能性减少。
本文章由计算机程序翻译，如有差异，请以英文原文为准。
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Human anti-NR1 autoantibodies induce synaptic pathology with functional relevant loss of postsynaptic NMDA receptors
We investigated the pathogenic role of anti-N-Methyl-D-aspartate receptor (NMDAR) antibodies in neurons and in a mouse model of autoimmune encephalitis using LSM and super-resolution microscopy. We found a functional reduction of synaptic NMDARs.
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Biophotonics Congress: Optics in the Life Sciences Congress 2019 (BODA,BRAIN,NTM,OMA,OMP)
Biophotonics Congress: Optics in the Life Sciences Congress 2019 (BODA,BRAIN,NTM,OMA,OMP)
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