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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 publication




Journal article


Ann Neurol

Publication Date





591 - 596


Adult, Animals, Botulinum Toxins, Type A, Cells, Cultured, Female, Ganglia, Spinal, Healthy Volunteers, Humans, Hyperalgesia, Male, Mechanotransduction, Cellular, Membrane Potentials, Mice, Inbred C57BL, Neuromuscular Agents, Pain Measurement, Pain Threshold, Patch-Clamp Techniques, Psychophysics, Sensory Receptor Cells, Young Adult