A reappraisal of the central effects of botulinum neurotoxin type A: by what mechanism?
Version of Record online: 19 JAN 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 109, Issue 1, pages 15–24, April 2009
How to Cite
Caleo, M., Antonucci, F., Restani, L. and Mazzocchio, R. (2009), A reappraisal of the central effects of botulinum neurotoxin type A: by what mechanism?. Journal of Neurochemistry, 109: 15–24. doi: 10.1111/j.1471-4159.2009.05887.x
- Issue online: 9 MAR 2009
- Version of Record online: 19 JAN 2009
- Received October 9, 2008; revised manuscript received and accepted January 8, 2009.
- botulinum neurotoxins;
- movement disorders;
- neuromuscular junction;
- retrograde axonal transport;
- synaptic transmission;
- synaptosomal-associated protein of 25-kDa
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.