AXONAL DEGENERATION ACCOMPANIED BY CONDUCTION BLOCK INDUCED BY TOXIN MEDIATED IMMUNE REACTIVITY TO GM1 GANGLIOSIDE IN RAT NERVES

Immune mechanisms have been implicated in the pathogenesis of motor ne uropathy with conduction blocks and of acute axonal neuropathy, and GM 1 ganglioside has been identified as a potential target antigen. In th ese experiments, the B subunit of cholera toxin (CT-B), which binds to GM1, was used to target an antibody response to GM1 in peripheral ner ve. CT-B was injected into the sciatic nerves of rats, in which anti-C T antibodies were previously induced by immunization, so that the circ ulating anti-CT-B antibodies bound to the CT-B-GM1 complex in the nerv e. Electrophysiological studies revealed the presence of conduction bl ock, and in pathological studies there was axonal degeneration with li ttle demyelination. Control animals, in which keyhole limpet hemocyani n was substituted for CT, did not develop conduction block or axonal d egeneration. These studies indicate that antibodies directed at GM1 si tes in peripheral nerve could cause an axonal neuropathy with conducti on block.