Abstract
Botulinum toxin type A, when applied to the extensor digitorum longus muscle of rats, reduces spontaneous and evoked transmitter release to a few per cent of the normal level. The toxin, however, fails to affect the morphological redifferentiation of the postsynaptic part of the neuromuscular junction following muscle degeneration-regeneration induced by a selective myotoxic agent, bupivacaine. This indicates that neither transmitter release nor resulting muscle activity are necessary for the differentiation of the sole plate.
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