Botulinum toxin type A reduces TRPV1 expression in the dorsal root ganglion in rats with adjuvant-arthritis pain

- The expression of TRPV1 receptors in DRG is related to nociceptive input in rats with adjuvant-arthritis pain.
- BoNT/A can play a role in DRG through its retrograde axonal transport.
- Antinociceptive effect of BoNT/A is associated with the inhibition of TRPV1 plasma membrane trafficking in DRG.

Arthritis pain affects people's long-term health, and recent studies have demonstrated that transient receptor potential vanilloid type 1 (TRPV1) plays a crucial role in arthritis pain. In addition, Pre-clinical evidence indicated that botulinum toxin type A (BoNT/A) has antinociceptive effect. The present study investigated the causality between the antinociceptive effects of BoNT/A and the expression of TRPV1 in dorsal root ganglion (DRG) in rats with adjuvant-arthritis pain. The results showed that BoNT/A significantly reduced adjuvant-arthritis nociceptive behaviors in a dose-dependent manner. Furthermore, the BoNT/A cleaved synaptosomal-associated protein of 25 kDa (cl-SNAP-25) was detected in the DRG using immunofluorescence after intra-articular administration. Although BoNT/A significantly reduced the protein levels of TRPV1, there were no significant changes in the mRNA levels of TRPV1 between CFA and BoNT/A (1U, 3U, 10U) group after BoNT/A retrograde axonal transport into the DRG with quantitative RT-PCR. This research provides evidence that the antinociceptive mechanism of BoNT/A might be mediated by reduction of TRPV1 expression through inhibition of its plasma membrane trafficking after intra-articular administration.