The mechanism of action of botulinum toxin A is best described by:

Presynaptic blockade of acetylcholine release Botulinum toxin is an effective inhibitor of presynaptic acetylcholine exocytosis. Acting at the neuromuscular junction, cellular uptake is believed to occur through an active cell surface receptor-mediated process. This three-step chemical denervation is initiated by the toxin selectively binding to sites on the surface membrane of cholinergic nerve endings. An energy-dependent endocytotic process ensues internalizing the cell membrane with bound protein. The final step is presumed to act on calcium-mediated exocytosis, preventing the release of acetylcholine into the synaptic cleft. It is also believed that Botulinum toxin acts as a zinc-dependent metalloendo protease to inhibit exocytosis.