The effect of Lambert-Eaton myasthenic syndrome antibody on slow action potentials in mouse cardiac ventricle

Abstract

Immunoglobulin G (IgG) from Lambert-Eaton myasthenic syndrome (LEMS) patients acts at motor nerve terminal Ca²⁺ channels. It was injected into mice to investigate effects on cardiac Ca²⁺ channels. Intracellular recordings were made of slow action potentials in right ventricular muscle cells in the presence of high K⁺ concentrations and isoprenaline (1µM). Reduction in Ca²⁺ concentration reduced the rate of rise and amplitude, but not the duration, of slow action potentials whereas verapamil (1µM) blocked them. They were not blocked by tetrodotoxin (10 µM), and 4-aminopyridine (1mM) prolonged the decay phase without affecting the rate of rise and amplitude. The rate of rise, amplitude and duration of slow action potentials were not affected by LEMS IgG. These results show that LEMS IgG does not act on Ca²⁺ channel currents that underlie slow action potentials in mouse ventricles, suggesting antigenic differences between Ca²⁺ channels at motor nerve terminals and heart.