Evidence for Anterograde Transport and Transcytosis of Botulinum Neurotoxin A (BoNT/A)

Botulinum toxin A, brain and pain

“…BoNT/A-truncated SNAP-25 re-occurred due to longer intracellular duration of proteolytic action of BoNT/A LC in comparison to BoNT/E LC (Antonucci et al, 2008;Keller and Neale, 1999). In a similar experiment it was demonstrated that BoNT/A protease was anterogradely transported and transcytosed to second-order synapses in superior colliculus (Restani et al, 2011). BoNT/A was injected into the retina and its proteolytic activity was demonstrated in optic tectum after 3 days.…”

Botulinum toxin type A selectivity for certain types of pain is associated with capsaicin-sensitive neurons

“…In present study we examined whether BoNT/A's enzymatic activity in the TNC is located in primary sensory In present experiments we did not observe any truncated SNAP-25 remaining after ganglionic denervation, thus, our results do not support possible transcytosis to second order synapses in the TNC. However, transcytosis of BoNT/A in rats was demonstrated after both anterograde and retrograde axonal transport in the optic system [52,53]. Recently, a decrease of spontaneous and evoked inhibitory glycinergic potentials in isolated rat lumbar substantia gelatinosa neurons following peripheral BoNT/A injection was reported [1].…”

Effects of botulinum toxin type A facial injection on monoamines and their metabolites in sensory, limbic and motor brain regions in rats

“…Beside the peripheral effects, BTX-A is known for its central effects, too. Studies in rodents show that the toxin is retrogradely transported and transcytosed to second-order neurons in the central 8 nervous system [2,3,37]. Also, studies in humans support the idea that BTX-A injected at therapeutic doses induces distant spinal and cortical effects indirectly by promoting brain changes due to plastic rearrangements subsequent to denervation or alterations in sensory input [22].…”