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<p>Despite its long-recognized effects in relieving pain, the neural substrates of auricular stimulation remain elusive. Here, we show that trans-auricular vagus nerve stimulation (taVNS), i.e., electrical stimulation of the auricular concha, effectively induces analgesia in a mouse model of neuropathic pain. Viral tracing, microendoscopic calcium imaging, and multi-electrode recordings reveal that auricular vagal signals travel to the jugular-nodose ganglia (JNG), which in turn connect to pro-opiomelanocortinergic neurons in nucleus tractus solitarius (NTS), subsequently activating glutamatergic neurons in ventrolateral periaqueductal gray (vlPAG). Optogenetic stimulation of central vagus terminals, JNG-derived auricular peripheral fibers, or vlPAG-projecting NTS neurons mimics taVNS-induced analgesia, whereas chemogenetic silencing of central vagus terminals or NTS neurons abolishes this effect. This study identifies an auricle–to–brain circuit underlying taVNS-driven analgesia in mice, with potential for facilitating taVNS optimization for pain management and other neurological conditions.</p>

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Auricular vagus nerve stimulation drives analgesia via an auricle–brain axis in a mouse model of neuropathic pain

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月21日

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  • Xiaoqi Peng,
  • Yehao Liu,
  • Yi Liu,
  • Yunfeng Mao,
  • Qianhui Xia,
  • An Liu,
  • Qian Dai,
  • Yingju Tai,
  • Bin Luo,
  • Hao Wang,
  • Yuanyin Wang,
  • Fang Kang,
  • Haitao Wang,
  • Zhi Zhang

摘要

Despite its long-recognized effects in relieving pain, the neural substrates of auricular stimulation remain elusive. Here, we show that trans-auricular vagus nerve stimulation (taVNS), i.e., electrical stimulation of the auricular concha, effectively induces analgesia in a mouse model of neuropathic pain. Viral tracing, microendoscopic calcium imaging, and multi-electrode recordings reveal that auricular vagal signals travel to the jugular-nodose ganglia (JNG), which in turn connect to pro-opiomelanocortinergic neurons in nucleus tractus solitarius (NTS), subsequently activating glutamatergic neurons in ventrolateral periaqueductal gray (vlPAG). Optogenetic stimulation of central vagus terminals, JNG-derived auricular peripheral fibers, or vlPAG-projecting NTS neurons mimics taVNS-induced analgesia, whereas chemogenetic silencing of central vagus terminals or NTS neurons abolishes this effect. This study identifies an auricle–to–brain circuit underlying taVNS-driven analgesia in mice, with potential for facilitating taVNS optimization for pain management and other neurological conditions.