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Anti‐GM1 antibodies can block neuronal voltage‐gated sodium channels
Author(s) -
Weber Frank,
Rüdel Reinhardt,
Aulkemeyer Peter,
Brinkmeier Heinrich
Publication year - 2000
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/1097-4598(200009)23:9<1414::aid-mus13>3.0.co;2-0
Subject(s) - antibody , sodium channel , chemistry , excitatory postsynaptic potential , guillain barre syndrome , complement system , biophysics , membrane potential , sodium , immunology , biochemistry , medicine , receptor , biology , organic chemistry
Anti‐GM1 antibodies, frequently found in the serum of patients with Guillain‐Barré syndrome (GBS), have been suggested to interfere with axonal function. We report that IgG anti‐GM1 antibodies, raised in rabbits, can reversibly block the voltage‐gated Na + channels of nerve cells, thus causing a reduction of the excitatory Na + current. The block was, however, only substantial when the antibodies were applied together with rabbit complement factors. A solution containing anti‐GM1 sera (dilution 1:100) and complement (1:50) reduced the Na + current to 0.5 ± 0.2 times control (mean value ± SD). Applications of the antibody by itself, complement by itself, or anti‐GM2 or anti‐GM4 antibodies (1:100) plus complement had little effect. The complexes of anti‐GM1 antibodies and complement factors block the ion‐conducting pore of the channel directly. In addition, they increase the fraction of channels that are inactivated at the resting potential and alter channel function by changing the membrane surface charge. The described effects may be responsible for conduction slowing and reversible conduction failure in some GBS patients. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1414–1420, 2000.