Botulinum Toxin-A Treatment Reduces Human Mechanical Pain Sensitivity and Mechanotransduction

Kathryn Paterson, Stephane Lolignier, John N. Wood, Stephen B. McMahon, David L. H. Bennett*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

44 Citations (Scopus)
62 Downloads (Pure)

Abstract

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.

Original languageEnglish
Pages (from-to)591-596
Number of pages6
JournalAnnals of Neurology
Volume75
Issue number4
Early online date18 Feb 2014
DOIs
Publication statusPublished - Apr 2014

Keywords

  • NEUROPATHIC PAIN
  • SENSORY NEURONS
  • SECONDARY HYPERALGESIA
  • EVOKED PAIN
  • MODEL
  • SENSITIZATION
  • NOCICEPTORS
  • EXOCYTOSIS
  • NEUROTOXIN
  • CAPSAICIN

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