Rats immunized with cholinergic synaptosomes: A model for Lambert‐Eaton syndrome

Joab Chapman, Ruth Rabinowitz, Amos D. Korczyn*, Daniel M. Michaelson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)726-733
Number of pages8
JournalMuscle and Nerve
Volume13
Issue number8
DOIs
StatePublished - Aug 1990

Funding

FundersFunder number
National Institute of Mental HealthR01MH040294

    Keywords

    • Lambert‐Eaton myasthenic syndrome
    • Torpedo
    • acetylcholine release
    • autoantibodies
    • electromyography

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