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A reappraisal of the central effects of botulinum neurotoxin type A: by what mechanism?
Author(s) -
Caleo Matteo,
Antonucci Flavia,
Restani Laura,
Mazzocchio Riccardo
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.05887.x
Subject(s) - neuroscience , botulinum neurotoxin , neurotoxin , neurology , acetylcholine , mechanism (biology) , motor nerve , chemistry , cleavage (geology) , medicine , pharmacology , biology , toxin , biochemistry , philosophy , epistemology , paleontology , fracture (geology)
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.