An animal model of Miller Fisher syndrome: Mitochondrial hydrogen peroxide is produced by the autoimmune attack of nerve terminals and activates Schwann cells
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- 作者：Umberto Rodellaa ; Michele Scorzetoa ; Elisa Duregottia ; Samuele Negroa ; Bryan C. Dickinsonb ; Christopher J. Changc ; d ; Nobuhiro Yukie ; Michela Rigonia ; rigonimic@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Cesare Montecuccoa ; f ; cesare.montecucco@gmail.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：Miller Fisher syndrome ; Neuromuscular junction ; Hydrogen peroxide ; ERK1/2 ; Schwann cells
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：96
- 期：Complete
- 页码：95-104
- 全文大小：2215 K
文摘
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Anti-GQ1b antibody plus complement reversibly damages motor axon terminals.
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A membrane attack complex forms at the neuronal surface in vitro and in vivo.
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Calcium overload and mitochondrial impairment take place in primary neurons.
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Neurons produce hydrogen peroxide in response to anti-GQ1b plus complement.
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Neuronal hydrogen peroxide activates ERK pathway in perisynaptic Schwann cells.