Differential blocking effects of the monoclonal anti-GQ1b IgM antibody and alpha-latrotoxin in the absence of complement at the mouse neuromuscular junction

被引：11

作者：

Buchwald, B ^{[1
]}

Ahangari, R ^{[1
]}

Toyka, KV ^{[1
]}

机构：

[1] Univ Wurzburg, Neurol Klin, D-97080 Wurzburg, Germany

来源：

NEUROSCIENCE LETTERS | 2002年 / 334卷 / 01期

关键词：

anti-GQ1b antibodies; CGM3; anti-ganglioside antibodies; Miller Fisher syndrome; Guillain-Barre syndrome; immune neuropathy; neuromuscular transmission;

D O I：

10.1016/S0304-3940(02)01037-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Numerous in vitro electrophysiological studies found different effects of anti-ganglioside antibodies on neuromuscular transmission. Since a complement-dependent, latrotoxin-like effect has been described for the mouse monoclonal anti-GQ1b IgM antibody (termed CGM3), we here investigated the effect of CGM3 and alpha-latrotoxin by means of the perfused macro-patch clamp electrode in mice hemidiaphragms in the absence of complement. The CGM3 mab depressed evoked quantal release dose-dependently, whereas the rate of spontaneous releases and the amplitude of postsynaptic currents was not significantly affected. Alpha-latrotoxin induced an increase in spontaneous releases followed by a blockade of evoked quantal release, this was not altered by CGM3. The complement-independent presynaptic block by CGM3 was different from the action of alpha-latrotoxin. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：25 / 28

页数：4

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