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This Article Free via Open Access: OA OA Full Text Full Text (PDF) OA All Versions of this Article: 586/13/3163    most recent jphysiol.2008.153569v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Rogozhin, A. A. Articles by Slater, C. R. PubMed PubMed Citation Articles by Rogozhin, A. A. Articles by Slater, C. R. Related Collections Neuroscience Related Article

¹ Kazan State Medical Academy, Kazan, Russia 420012
² Institute of Neuroscience, Newcastle University, UK
³ Kazan Institute of Biochemistry and Biophysics, Kazan, Russia 420111

Botulinum neurotoxin type A (BoNT/A) paralyses muscles by blocking acetylcholine (ACh) release from motor nerve terminals. Although highly toxic, it is used clinically to weaken muscles whose contraction is undesirable, as in dystonias. The effects of an injection of BoNT/A wear off after 3–4 months so repeated injections are often used. Recovery of neuromuscular transmission is accompanied by the formation of motor axon sprouts, some of which form new synaptic contacts. However, the functional importance of these new contacts is unknown. Using intracellular and focal extracellular recording we show that in the mouse epitrochleoanconeus (ETA), quantal release from the region of the original neuromuscular junction (NMJ) can be detected as soon as from new synaptic contacts, and generally accounts for > 80% of total release. During recovery the synaptic delay and the rise and decay times of endplate potentials (EPPs) become prolonged approximately 3-fold, but return to normal after 2–3 months. When studied after 3–4 months, the response to repetitive stimulation at frequencies up to 100 Hz is normal. When two or three injections of BoNT/A are given at intervals of 3–4 months, quantal release returns to normal values more slowly than after a single injection (11 and 15 weeks to reach 50% of control values versus 6 weeks after a single injection). In addition, branching of the intramuscular muscular motor axons, the distribution of the NMJs and the structure of many individual NMJs remain abnormal. These findings highlight the plasticity of the mammalian NMJ but also suggest important limits to it.

(Received 5 March 2008; accepted after revision 7 May 2008; first published online 8 May 2008)
Corresponding author C. R. Slater: Institute of Neuroscience, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK. Email: c.r.slater{at}ncl.ac.uk

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				C.-P. Ko Do nerve terminal sprouts contribute to functional recovery from botulinum neurotoxin A? J. Physiol., July 1, 2008; 586(13): 3021 - 3021. [Full Text] [PDF]