A reappraisal of the central effects of botulinum neurotoxin type A: by what mechanism?

被引：69

作者：

Caleo, Matteo ^{[1
]}

Antonucci, Flavia ^{[1
]}

Restani, Laura ^{[2
]}

Mazzocchio, Riccardo ^{[3
]}

机构：

[1] CNR, Ist Neurosci, I-56100 Pisa, Italy

[2] Scuola Normale Super Pisa, Pisa, Italy

[3] Univ Siena, Sez Neurofisiol Clin, Dipartimento Sci Neurol Neurochirurg & Comportame, I-53100 Siena, Italy

来源：

JOURNAL OF NEUROCHEMISTRY | 2009年 / 109卷 / 01期

关键词：

botulinum neurotoxins; movement disorders; neuromuscular junction; retrograde axonal transport; synaptic transmission; synaptosomal-associated protein of 25-kDa; CENTRAL-NERVOUS-SYSTEM; TOXIN TYPE-A; ABDUCENS MOTONEURONS; RENSHAW CELLS; RECIPROCAL INHIBITION; RETROGRADE TRANSPORT; SKELETAL-MUSCLE; TROPHIC FACTORS; WRITERS CRAMP; RECOVERY;

D O I：

10.1111/j.1471-4159.2009.05887.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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.

引用

页码：15 / 24

页数：10

共 96 条

[1]

Neurophysiological effects of botulinum toxin type A [J].