Knock-down of Annexin A10 in trigeminal ganglion attenuates trigeminal neuropathic pain in mice

Abstract

Abstract Trigeminal neuropathic pain (TNP) is an intense chronic orofacial pain syndrome, which the pathogenesis and treatment of it are still limited (Cruccu et al. 2020; Yadav et al. 2017). We induced TNP from adult male mice via partial infraorbital nerve ligation (pIONL)(Xu et al. 2008). The upregulated genes were screened in the trigeminal ganglion (TG) 7 days after pIONL and found that Annexin A10 (Anxa10) mRNA was up-regulated by up to 19-fold. PIONL induced persistent upregulation of Anxa10 mRNA and protein in trigeminal ganglion (TG). In addition, Anxa10 colocalized with the astrocyte marker glial fibrillary acidic protein (GFAP), the neuronal marker TUJ1 and with the microglial marker IB4. To knock-down of Anxa10 expression, lentivirus containing Anxa10-shRNA (LV-Anxa10-shRNA) was microinjected into TG, and successful infection of the lentivirus was verified by immunofluorescence. After inhibiting Anxa10, the mechanical pain threshold of pIONL mice decreased accompanied decreasing of TNF-α and IL-1β. Also, whole-cell patch-clamp recording showed that knock-down of Anxa10 suppressed nerve injury-induced hyperexcitation of TG neurons. In conclusion, Anxa10 is participated in the maintenance of trigeminal neuropathic pain, and we try to explore more about trigeminal neuropathic pain in the future.