Type A1 but Not Type A2 Botulinum Toxin Decreases the Grip Strength of the Contralateral Foreleg Through Axonal Transport From the Toxin-Treated Foreleg of Rats

DOI Web Site 被引用文献6件 参考文献55件
  • Torii Yasushi
    The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN), Japan
  • Akaike Norio
    Research Division for Life Science, Kumamoto Health Science University, Japan
  • Harakawa Tetsuhiro
    The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN), Japan
  • Kato Keiko
    Department of Animal Medical Sciences, Kyoto Sangyo University, Japan
  • Sugimoto Nakaba
    Department of Molecular Therapeutics, Medical School of Osaka University, Japan
  • Goto Yoshitaka
    The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN), Japan
  • Nakahira Shinji
    The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN), Japan
  • Kohda Tomoko
    Department of Veterinary Sciences, School of Life and Environmental Sciences, Osaka Prefecture University, Japan
  • Kozaki Shunji
    Department of Veterinary Sciences, School of Life and Environmental Sciences, Osaka Prefecture University, Japan
  • Kaji Ryuji
    School of Medicine, University of Tokushima Faculty of Medicine, Japan
  • Ginnaga Akihiro
    The Chemo-Sero-Therapeutic Research Institute (KAKETSUKEN), Japan

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The adverse effects of botulinum LL toxin and neurotoxin produced by subtype A1 (A1LL and A1NTX) are becoming issues, as the toxins could diffuse from the toxin-treated (ipsilateral) to contralateral muscles. We have attempted to produce neurotoxin from subtype A2 (A2NTX) with an amino acid sequence different from that of neurotoxin subtype A1. We measured the grip strength on the contralateral foreleg as an indicator of toxin spread from the ipsilateral to contralateral muscles. Doses of 0.30 log U or above of A1LL and A1NTX reduced the contralateral grip strength, whereas a dose of 0.78 log U of A2NTX was required to do so. We investigated the route of toxin spread using denervated, colchicine-treated, and antitoxin-treated rats. A1LL was transported via axons at doses higher than 0.30 log U and via both axons and body fluid at about 0.80 log U or a higher dose. Interestingly, A2NTX was transported via body fluid at about 0.80 log U or a higher dose, but not via axons to the contralateral side. It was concluded that A1LL and A1NTX decreased the grip strength of the toxin-untreated foreleg via both axonal transport and body fluids, while A2NTX was only transported via the body fluid.

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