Failure of anti-GM1 IgG or IgM to induce conduction block following intraneural transfer.
In order to confirm the reported pathogenicity of human antibodies to monosialoganglioside GM1, immunoglobulin fractions with high anti-GM1 IgG or IgM titers were prepared from patients with Guillain-Barré syndrome and multifocal motor neuropathy respectively. These fractions were injected intraneurally into rat tibial nerves with fresh human complement. Neither the anti-GM1 IgG nor the anti-GM1 IgM fraction induced significant focal conduction block or slowing compared to a pooled fraction prepared from 5 normal individuals. In contrast, rabbit experimental allergic neuritis serum included as a positive control was highly active. Transverse sections of injected nerve failed to show evidence of demyelination. Staining for human immunoglobulin in cryostat sections showed the presence of injected anti-GM1 antibody bound to nodes of Ranvier up to 6 days following intraneural transfer. These data fail to confirm previous reports of conduction block from intraneural transfer of anti-GM1 serum and suggest that such electrophysiological effects may be the result of factors other than or in addition to anti-GM1 antibodies.
Harvey
G K
GK
Department of Neurology, Julius-Maximillians-Universität, Wurzburg, Germany.
Toyka
K V
KV
Zielasek
J
J
Kiefer
R
R
Simonis
C
C
Hartung
H P
HP
D000818:Animals; D000906:Antibodies / Q000032:analysis / Q000494:pharmacology*; D005260:Female; D005677:G(M1) Ganglioside / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology*; D007075:Immunoglobulin M / Q000494:pharmacology*; D009431:Neural Conduction; D009468:Neuromuscular Diseases / Q000276:immunology* / Q000503:physiopathology*; D051381:Rats
D000906:Antibodies; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D005677:G(M1) Ganglioside