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. 1987 Sep;390:257–270. doi: 10.1113/jphysiol.1987.sp016698

The effect of myasthenic syndrome antibody on presynaptic calcium channels in the mouse.

B Lang 1, J Newsom-Davis 1, C Peers 1, C Prior 1, D W Wray 1
PMCID: PMC1192178  PMID: 2450991

Abstract

1. The action of immunoglobulin G obtained from patients with Lambert-Eaton myasthenic syndrome (LEMS IgG) was investigated by injecting mice, followed by intracellular recordings from the mouse diaphragm. 2. End-plate potential quantal content was studied over a range of Ca2+ concentrations. Curves of log quantal content versus log Ca2+ concentration were shifted to the right by LEMS IgG. For low Ca2+ concentrations, release continued to follow Poisson statistics after LEMS IgG treatment. 3. Miniature end-plate potential (m.e.p.p.) frequency was measured in solutions containing high K+ concentrations. LEMS IgG significantly reduced m.e.p.p. frequency at each K+ concentration studied. 4. M.e.p.p. frequency was measured at fixed high-K+ concentration (15.9 mM) for a range of Ca2+ concentrations. The log-log plot of m.e.p.p. frequency versus Ca2+ concentration was shifted downwards throughout by LEMS IgG. 5. M.e.p.p. frequency was not affected by LEMS IgG in Ca2+-free solutions (K+ concentration 15.9 mM) or in solutions of low Ca2+ concentration (K+ concentration 5.9 mM). 6. At each Ca2+ concentration studied, m.e.p.p. amplitudes were not affected by LEMS IgG. 7. The data suggest that LEMS IgG acts on presynaptic voltage-dependent Ca2+ channels to cause their loss of function, probably by down-regulation.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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