Inhibition of Membrane Na⁺ Channels by A Type Botulinum Toxin at Femtomolar Concentrations in Central and Peripheral Neurons

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  • Shin Min-Chul
    Research Division for Life Sciences, Kumamoto Health Science University, Japan
  • Wakita Masahito
    Research Division for Life Sciences, Kumamoto Health Science University, Japan
  • Xie Du-Jie
    Research Division for Life Sciences, Kumamoto Health Science University, Japan Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Japan
  • Yamaga Toshitaka
    Research Division for Life Sciences, Kumamoto Health Science University, Japan Department of Brain Science and Engineering, Kyushu Institute of Technology, Japan
  • Iwata Satomi
    Research Division for Life Sciences, Kumamoto Health Science University, Japan
  • Torii Yasushi
    Human Vaccine Production Department, The Chemo-Sero-Therapeutic Research Institute, Japan
  • Harakawa Tetsuhiro
    Human Vaccine Production Department, The Chemo-Sero-Therapeutic Research Institute, Japan
  • Ginnaga Akihiro
    Human Vaccine Production Department, The Chemo-Sero-Therapeutic Research Institute, Japan
  • Kozaki Shunji
    Laboratory of Veterinary Epidemiology, Department of Veterinary Science, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, Japan
  • Akaike Norio
    Research Division for Life Sciences, Kumamoto Health Science University, Japan

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  • Inhibition of Membrane Na<SUP>+</SUP> Channels by A Type Botulinum Toxin at Femtomolar Concentrations in Central and Peripheral Neurons

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Recent studies have demonstrated that the botulinum neurotoxins inhibit the release of acetylcholine, glutamate, GABA, and glycine in central nerve system (CNS) neurons. The Na+ current (INa) is of major interest because it acts as the trigger for many cellular functions such as transmission, secretion, contraction, and sensation. Thus, these observations raise the possibility that A type neurotoxin might also alter the INa of neuronal excitable membrane. To test our idea, we examined the effects of A type neurotoxins on INa of central and peripheral neurons. The neurotoxins in femtomolar to picomolar concentrations produced substantial decreases of the neuronal INa, but interestingly the current inhibition was saturated at about maximum 50% level of control INa. The inhibitory pattern in the concentration–response curve for the neurotoxins differed from tetrodotoxin (TTX), local anesthetic, and antiepileptic drugs that completely inhibited INa in a concentration-dependent manner. We concluded that A type neurotoxins inhibited membrane Na+-channel activity in CNS neurons and that INa of both TTX-sensitive and -insensitive peripheral dorsal ganglion cells were also inhibited similarly to a maximum 40% of the control by the neurotoxins. The results suggest evidently that A2NTX could be also used as a powerful drug in treating epilepsy and several types of pain.

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