Botulinum toxin type A mechanism: current hypothesis. At the nerve terminal, botulinum toxin type A is thought to induce a temporary chemodenervation through the following steps:

1. The toxin binds to acceptors (yet to be identified) on cholinergic terminals (arrow indicates a BTX-A molecule).
2. The molecule is internalized into the nerve ending. 
3. Once inside the nerve ending, botulinum toxin interferes with the exocytosis of cholinergic vesicles. This leads to chemodenervation and reduced muscular contractions.
4. Over time, terminal sprouting occurs. 
5. Finally, the original functional endplate is re-established and sprouts regress (as reported by Prof. Oliver Dolly’s laboratory). At this point symptoms may return in some patients. 

Note: Data obtained from murine neuromuscular junction after a single BTX-A treatment revealed that the original endplate became reactivated as the sprouts regressed (dePaiva et al, 1999).

dePaiva A, Meunier FA, Molgo J, Aoki KR, Dolly JO. Functional repair of motor endplates after botulinum neurotoxin type A poisoning: biphasic switch of synaptic activity between nerve sprouts and their parent terminals. Proc Natl Acad Sci 1999;96:3200-5.