Literature DB >> 7905957

Serum factor in Miller-Fisher variant of Guillain-Barré syndrome and neurotransmitter release.

M Roberts1, H Willison, A Vincent, J Newsom-Davis.   

Abstract

Serum IgG autoantibodies to GQ1b ganglioside are associated with the acute phase of the Miller-Fisher syndrome (MFS). We investigated the effects of three anti-GQ1b-positive MFS sera in the mouse phrenic-nerve/diaphragm preparation. Miniature endplate potential frequencies increased eight-fold within 25 min, declined rapidly, and ceased altogether after 3 h, when nerve stimulation no longer evoked a response. One MFS convalescent serum (anti-GQ1b negative) and sera from healthy controls and from patients with other neurological diseases were without effect. Thus muscle weakness in MFS may be caused by a serum factor, likely to be GQ1b antibody, that leads to failure of acetylcholine release from motor nerve terminals.

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Year:  1994        PMID: 7905957     DOI: 10.1016/s0140-6736(94)92694-8

Source DB:  PubMed          Journal:  Lancet        ISSN: 0140-6736            Impact factor:   79.321


  20 in total

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Review 8.  Complex gangliosides as autoantibody targets at the neuromuscular junction in Miller Fisher syndrome: a current perspective.

Authors:  Graham M O'Hanlon; Roland W M Bullens; Jaap J Plomp; Hugh J Willison
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9.  Complex gangliosides at the neuromuscular junction are membrane receptors for autoantibodies and botulinum neurotoxin but redundant for normal synaptic function.

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10.  Synaptic function of cholinergic-specific Chol-1alpha ganglioside.

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