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Journal Article

IgG from Patients with Lambert-Eaton Syndrome Blocks Voltage-Dependent Calcium Channels


Neher,  E.
Department of Membrane Biophysics, MPI for biophysical chemistry, Max Planck Society;

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Kim, Y. I., & Neher, E. (1988). IgG from Patients with Lambert-Eaton Syndrome Blocks Voltage-Dependent Calcium Channels. Science, 239(4838), 405-408. doi:10.1126/science.2447652.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002D-EE15-F
Lambert-Eaton syndrome, an autoimmune disorder frequently associated with small-cell carcinoma of the lung, is characterized by impaired evoked release of acetylcholine from the motor nerve terminal. Immunoglobulin G (IgG) antibodies from patients with the syndrome, applied to bovine adrenal chromaffin cells, reduced the voltage-dependent calcium channel currents by about 40 percent. When calcium was administered directly into the cytoplasm, however, the IgG-treated cells exhibited normal exocytotic secretion, as assayed by membrane capacitance measurement. Measurement with the fluorescent calcium indicator fura-2 indicated that the IgG treatment reduced potassium-stimulated increase in free intracellular calcium concentration. The pathogenic IgG modified neither kinetics of calcium channel activation nor elementary channel activity, suggesting that a reduction in the number of functional calcium channels underlies the IgG-induced effect. Therefore, Lambert-Eaton syndrome IgG reacts with voltage-dependent calcium channels and blocks their function, a phenomenon that can account for the presynaptic impairment characteristic of this disorder.