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α‐Bungarotoxin sensitization in experimental autoimmune myasthenia gravis
Author(s) -
Kennel Philippe F.,
Poindron Philippe,
Warter JeanMarie,
Fonteneau Paul
Publication year - 1993
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/mus.880160505
Subject(s) - myasthenia gravis , acetylcholine receptor , neuromuscular transmission , neuromuscular junction , medicine , sensitization , acetylcholine , immunology , weakness , stimulation , immunization , antibody , receptor , anesthesia , biology , neuroscience , anatomy
A mouse model of MG, termed experimental autoimmune myasthenia gravis (EAMG), can be obtained after immunization with Torpedo acetylcholine receptor (AChR). Although many studies have detailed the consequence of AChR antibodies binding at the neuromuscular junction and the difficulty in obtaining obvious clinical signs, less attention has been focused on the possibility of amplifying the muscular block in order to discriminate between immunized and healthy animals. In the present studies we observe that a single inoculation of α‐bungarotoxin (α‐bgt) can amplify the neuromuscular block revealed by repetitive nerve stimulation, and induce in EAMG mice a stable muscular weakness state lasting for at least 169 hours instead of 95 hours in normal mice. This model could provide an excellent tool for evaluating drugs active on neuromuscular transmission. © 1993 John Wiley & Soncs, Inc.