Lambert-Eaton syndrome seems to be caused by circulating antibodies to voltage gated calcium channels. Calcium entry into the nerve terminal during depolarisation is reduced with a consequent reduction in the number of quanta of acetylcholine released.
The spontaneous release of quanta by exocytosis is not affected. Hence, during repetitive stimulation the end plate potential is allowed to increase before an action potential is finally triggered. This explains the initial augmentation of strength during a voluntary contraction.
Cells of the tumour can be shown to have voltage gated calcium channels. The association of small cell lung carcinoma with the Lambert Eaton syndrome is thought to result from an initial auto- antibody response to block the channels on the tumour cells, with secondary blockade of normal nerve terminals.
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