bioRxiv : the preprint server for biology · 2025
Injured SSTR2 + nociceptor axons in neuromas drive chronic spontaneous neuropathic pain.
СтатьяПрепринтНазвание и аннотация: Перевод в очереди
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Zeng Xiangsunze, Martinez-Garcia Rosa I, Bhuiyan Shamsuddin A, Heo Keunjung, MacKinnon-Booth Natalie, Bentley Elke, Shea Emily, Wu Kangling, Barkai Omer, Turnes Bruna Lenfers, Jayakar Selwyn S, Gomez-Eslava Barbara, Hameed Mustafa Q, Santiago Celine, Lezgiyeva Karina, Osei-Asante Emmanuella, Furfaro Ivan, Rotenberg Alexander, Johnston Benjamin R, Wainger Brian J, Renthal William, Lacour Stéphanie P, Ginty David D, Woolf Clifford J
Аннотация
Spontaneous pain is a very common but poorly understood consequence of peripheral nerve injury. We developed a system for measuring spontaneous pain-related behaviors in mice over months, which revealed that limb flicks-emerging predominantly 2 months post-injury-reflect spontaneous pain, and that neuromas are the drivers of this component of neuropathic pain. In vivo dorsal root ganglion imaging showed that small-diameter sensory neurons are the source of spontaneous ectopic neuroma activity and are different from the intact neurons that drive stimulus-evoked pain. Cell-specific optogenetic stimulation studies identified that injured SSTR2 + sensory axons in neuromas are the triggers of spontaneous limb flicks/neuropathic pain. These findings reveal the mechanisms of spontaneous neuropathic pain and open new therapeutic opportunities.