Botulinum toxin-A treatment reduces human mechanical pain sensitivity and mechanotransduction

Ann Neurol. 2014 Apr;75(4):591-6. doi: 10.1002/ana.24122. Epub 2014 Mar 13.


The mechanisms underlying the analgesic effects of botulinum toxin serotype A (BoNT-A) are not well understood. We have tested the hypothesis that BoNT-A can block nociceptor transduction. Intradermal administration of BoNT-A to healthy volunteers produced a marked and specific decrease in noxious mechanical pain sensitivity, whereas sensitivity to low-threshold mechanical and thermal stimuli was unchanged. BoNT-A did not affect cutaneous innervation. In cultured rodent primary sensory neurons, BoNT-A decreased the proportion of neurons expressing slowly adapting mechanically gated currents linked to mechanical pain transduction. Inhibition of mechanotransduction provides a novel locus of action of BoNT-A, further understanding of which may extend its use as an analgesic agent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Botulinum Toxins, Type A / pharmacology*
  • Botulinum Toxins, Type A / therapeutic use*
  • Cells, Cultured
  • Female
  • Ganglia, Spinal / cytology
  • Healthy Volunteers
  • Humans
  • Hyperalgesia / drug therapy*
  • Male
  • Mechanotransduction, Cellular / drug effects*
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Mice, Inbred C57BL
  • Neuromuscular Agents / pharmacology
  • Neuromuscular Agents / therapeutic use
  • Pain Measurement
  • Pain Threshold / drug effects*
  • Patch-Clamp Techniques
  • Psychophysics
  • Sensory Receptor Cells / drug effects
  • Young Adult


  • Neuromuscular Agents
  • Botulinum Toxins, Type A