| First Author | Deseure K | Year | 2026 |
| Journal | Cell Rep Med | Volume | 7 |
| Issue | 3 | Pages | 102645 |
| PubMed ID | 41806836 | Mgi Jnum | J:383164 |
| Mgi Id | MGI:8322302 | Doi | 10.1016/j.xcrm.2026.102645 |
| Citation | Deseure K, et al. (2026) TRPM3 mediates spontaneous pain and mechanical allodynia in a mouse model of chronic orofacial neuropathy. Cell Rep Med 7(3):102645 |
| abstractText | Trigeminal nerve injury can lead to chronic and difficult-to-treat orofacial neuropathic pain. Here, we uncover a key role for the cation channel TRPM3 in the chronic constriction injury of the infraorbital nerve (IoN-CCI) mouse model of trigeminal neuropathic pain. Wild-type (WT) mice develop spontaneous pain and mechanical allodynia for up to 6 weeks following IoN-CCI, whereas Trpm3(-/-) mice do not develop such symptoms. Using longitudinal RNA sequencing (RNA-seq) analysis, we obtain a detailed time course of transcriptome alterations in trigeminal ganglia during progression of the IoN-CCI model; notably, gene expression regulation is not different between WT and Trpm3(-/-) mice. Two structurally distinct TRPM3 antagonists, primidone and isosakuranetin, effectively reverse spontaneous pain and mechanical allodynia, whereas mavatrep, a potent TRPV1 antagonist, is without analgesic effect. These data indicate that TRPM3 is essential for ongoing pain and allodynia following trigeminal nerve injury, making it a potential target for treating trigeminally mediated neuropathic pain. |
