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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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 Rodella^a ; Michele Scorzeto^a ; Elisa Duregotti^a ; Samuele Negro^a ; Bryan C. Dickinson^b ; Christopher J. Chang^c ; ^d ; Nobuhiro Yuki^e ; Michela Rigoni^a ; ^{rigonimic@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; Cesare Montecucco^a ; ^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

•: Anti-GQ1b antibody plus complement reversibly damages motor axon terminals.
•: A membrane attack complex forms at the neuronal surface in vitro and in vivo.
•: Calcium overload and mitochondrial impairment take place in primary neurons.
•: Neurons produce hydrogen peroxide in response to anti-GQ1b plus complement.
•: Neuronal hydrogen peroxide activates ERK pathway in perisynaptic Schwann cells.