ABSTRACT
Lambert-Eaton syndrome (LES) is a rare acquired autoimmune disease in which pathogenic autoantibodies are directed against the voltage-gated calcium channels (VGCCs) on the presynaptic nerve terminal. As discussed inChapter 1, the opening of these calcium channels is required for the influx of calcium into the presynaptic terminal, which leads to the exocytosis of synaptic vesicles and the release of acetylcholine. The pathogenic VGCC antibodies compromise presynaptic function by impairing the quantal release of acetylcholine.
