A reappraisal of the central effects of botulinum neurotoxin type A: by what mechanism?
Botulinum neurotoxin A (BoNT/A) is a metalloprotease that enters peripheral motor nerve terminals and blocks the release of acetylcholine via the specific cleavage of the synaptosomal-associated protein of 25-kDa. Localized injections of BoNT/A are widely employed in clinical neurology to treat several human diseases characterized by muscle hyperactivity. It is generally assumed that the effects of BoNT/A remain localized to the injection site. However, several neurophysiological studies have provided evidence for central effects of BoNT/A, raising the issue of how these actions arise. Here we review these data and discuss the possibility that retrograde axonal transport of catalytically active BoNT/A may explain at least some of its effects at the level of central circuits.
Caleo
Matteo
M
Istituto di Neuroscienze, Consiglio Nazionale delle Ricerche, Pisa, Italy. caleo@in.cnr.it
Antonucci
Flavia
F
Restani
Laura
L
Mazzocchio
Riccardo
R
D000818:Animals; D001370:Axonal Transport / Q000187:drug effects / Q000502:physiology; D019274:Botulinum Toxins, Type A / Q000008:administration & dosage* / Q000493:pharmacokinetics / Q000502:physiology*; D002384:Catalysis; D002490:Central Nervous System / Q000187:drug effects* / Q000378:metabolism*; D006801:Humans; D007273:Injections, Intramuscular; D009468:Neuromuscular Diseases / Q000188:drug therapy / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism
D019274:Botulinum Toxins, Type A