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 language | English |
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Pages (from-to) | 591-596 |
Number of pages | 6 |
Journal | Annals of Neurology |
Volume | 75 |
Issue number | 4 |
Early online date | 18 Feb 2014 |
DOIs | |
Publication status | Published - Apr 2014 |
Keywords
- NEUROPATHIC PAIN
- SENSORY NEURONS
- SECONDARY HYPERALGESIA
- EVOKED PAIN
- MODEL
- SENSITIZATION
- NOCICEPTORS
- EXOCYTOSIS
- NEUROTOXIN
- CAPSAICIN