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    Ablation of TRPV11 afferent terminals by capsaicin mediates long-lasting analgesia for trigeminal neuropathic pain

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    Author
    Wang, S.
    Bian, C.
    Yang, J.
    Arora, V.
    Gao, Y.
    Wei, F.
    Chung, M.-K.
    Date
    2020
    Journal
    eNeuro
    Publisher
    Society for Neuroscience
    Type
    Article
    
    Metadata
    Show full item record
    See at
    http://doi.org/10.1523/ENEURO.0118-20.2020
    Abstract
    Trigeminal 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.
    Sponsors
    This work was supported by National Institutes of Health Grants DE023846 and DE027731.
    Keyword
    Analgesia
    Capsaicin
    Neuropathic pain
    Orofacial pain
    TRPV1
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085618371&doi=10.1523%2fENEURO.0118-20.2020&partnerID=40&md5=ef6deeae59ebbfb9fed1f05c8a5d5cfe; http://hdl.handle.net/10713/12995
    ae974a485f413a2113503eed53cd6c53
    10.1523/ENEURO.0118-20.2020
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    UMB Open Access Articles 2020

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