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Rats immunized with cholinergic synaptosomes: A model for Lambert‐Eaton syndrome
Author(s) -
Chapman Joab,
Rabinowitz Ruth,
Korczyn Amos D.,
Michaelson Daniel M.
Publication year - 1990
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.880130811
Subject(s) - cholinergic , torpedo , neuromuscular transmission , neuromuscular junction , lambert eaton myasthenic syndrome , acetylcholine , myasthenia gravis , postsynaptic potential , neuroscience , medicine , neurotransmission , acetylcholine receptor , motor nerve , motor endplate , chemistry , endocrinology , immunology , biology , receptor
Lambert‐Eaton myasthenic syndrome (LEMS) is an autoimmune disorder characterized by reduced acetylcholine release at the neuromuscular junction. We report a model of the disease developed by active immunization of rats with purely cholinergic nerve terminals (synaptosomes) isolated from the Torpedo electric organ. Electromyographic studies of neuromuscular transmission in these rats showed a weak initial response followed by a pronounced incremental response to paired supramaximal stimuli (8 msec apart). There was no such response in control rats. There was no evidence of a postsynaptic transmission deficit in the synaptosomes immunized rats. We conclude that immunizing rats with Torpedo cholinergic nerve terminals causes a specific presynaptic dysfunction and may serve as a model for the study of LEMS.