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dc.contributor.authorWang, S.
dc.contributor.authorBian, C.
dc.contributor.authorYang, J.
dc.contributor.authorArora, V.
dc.contributor.authorGao, Y.
dc.contributor.authorWei, F.
dc.contributor.authorChung, M.-K.
dc.date.accessioned2020-06-08T20:21:01Z
dc.date.available2020-06-08T20:21:01Z
dc.date.issued2020
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85085618371&doi=10.1523%2fENEURO.0118-20.2020&partnerID=40&md5=ef6deeae59ebbfb9fed1f05c8a5d5cfe
dc.identifier.urihttp://hdl.handle.net/10713/12995
dc.description.abstractTrigeminal neuropathic pain (TNP) is often resistant to current pharmacotherapy, and there is a pressing need to develop more efficacious treatments. Capsaicin is a pungent ingredient of chili peppers and specifically activates transient receptor potential vanilloid subtype 1 (TRPV1), a Ca21-permeable ion channel. Topical capsaicin invariably induces burning pain. Paradoxically, the transient pain is often followed by prolonged attenuation of the preexisting pathologic pain from the same region. However, the mechanisms underlying capsaicin-induced analgesia are not well understood. Although the reports of the involvement of TRPV1 and TRPV11 afferents in neuropathic pain are controversial, we recently demonstrated that TRPV1 and TRPV11 afferents are involved in mechanical hyperalgesia in mice with chronic constriction injury of the infraorbital nerve (ION-CCI). Consistently, chemogenetic inhibition of TRPV1-lineage (TRPV1-LN) afferents attenuated mechanical hyperalgesia and ongoing pain. In mice with ION-CCI, we found that a single focal injection of capsaicin into facial skin led to attenuation of mechanical hyperalgesia over two weeks. Capsaicin treatment also attenuated secondary hyperalgesia in extraterritorial mandibular skin. Furthermore, capsaicin treatment decreased ongoing pain. Longitudinal in vivo two-photon imaging of cutaneous nerve fibers showed that such capsaicin-induced analgesia is correlated with cutaneous nerve terminal density. Furthermore, preventing capsaicin-induced ablation of afferent terminals by co-administration of capsaicin with MDL28170, an inhibitor of calpain, abolished capsaicin-induced analgesia. These results suggest that a single focal injection of capsaicin induces long-lasting analgesia for neuropathic pain via selective ablation of TRPV11 afferent terminals and that TRPV11 afferents contribute to the maintenance of TNP.en_US
dc.description.sponsorshipThis work was supported by National Institutes of Health Grants DE023846 and DE027731.en_US
dc.description.urihttp://doi.org/10.1523/ENEURO.0118-20.2020en_US
dc.language.isoen_USen_US
dc.publisherSociety for Neuroscienceen_US
dc.relation.ispartofeNeuro
dc.subjectAnalgesiaen_US
dc.subjectCapsaicinen_US
dc.subjectNeuropathic painen_US
dc.subjectOrofacial painen_US
dc.subjectTRPV1en_US
dc.titleAblation of TRPV11 afferent terminals by capsaicin mediates long-lasting analgesia for trigeminal neuropathic painen_US
dc.typeArticleen_US
dc.identifier.doi10.1523/ENEURO.0118-20.2020
dc.identifier.pmid32404326


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