Dimethyl Trisulfide Diminishes Traumatic Neuropathic Pain Acting on TRPA1 Receptors in Mice

Pharmacotherapy of neuropathic pain is still challenging. Our earlier work indicated an analgesic effect dimethyl trisulfide (DMTS), which was mediated by somatostatin released from nociceptor nerve endings acting on SST4 receptors. Somatostatin release occurred due to TRPA1 ion channel activation. In the present study, we investigated DMTS in evoked partial ligation sciatic mice. Expression mRNA Trpa1 murine dorsal-root-ganglion neurons detected RNAscope. Involvement channels and receptors tested with gene-deleted animals. Macrophage activity at site lesion determined lucigenin bioluminescence. Density activation microglia spinal cord dorsal horn verified immunohistochemistry image analysis. expressed peptidergic non-peptidergic root ganglion. ameliorated Sstr4 WT mice, but not KO ones. had no macrophage around damaged nerve. Microglial density reduced independently TRPA1. No microglial detected. might offer a novel therapeutic opportunity complementary treatment pain.