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<p>Attention distraction mitigates pain, yet its neural basis remains elusive. We established cricket hunting as an attention-demanding paradigm that alleviates acute and chronic pain in male mice. Activity tagging revealed that cricket hunting activated a subset of glutamatergic neurons in the superior colliculus (SC). Selective stimulation of these hunting-activated neurons alleviated chronic hyperalgesia, primarily mediated by their projections to the zona incerta (ZI). Notably, repeated engagement, either through the hunting paradigm or by repeatedly activating hunting-activated SC-ZI projections, induced sustained analgesia (lasting at least 6 hours), linked to potentiated glutamatergic inputs to ZI GABAergic neurons. Furthermore, SC-ZI projections originating from SC neurons expressing tachykinin precursor 1 (Tac1) selectively elevated neuropathic pain thresholds via substance P release and neurokinin 1 (NK1) receptor-dependent excitatory synaptic transmission onto ZI GABAergic neurons. Together, we show that a specific SC-ZI circuit drives attention-induced analgesia, highlighting the SC<sup>Tac1</sup>-ZI pathway as a therapeutic target for chronic pain.</p>

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An attention-demanding hunting paradigm engages the superior colliculus–zona incerta circuit mediating analgesia in male mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月19日

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  • Xue Zhang,
  • Xiao-Juan Liu,
  • Cui Yin,
  • Qiangqiang Zhou,
  • Jiaqi Zhang,
  • Liwei Wang,
  • Jun-Li Cao,
  • Cheng Xiao,
  • Chunyi Zhou

摘要

Attention distraction mitigates pain, yet its neural basis remains elusive. We established cricket hunting as an attention-demanding paradigm that alleviates acute and chronic pain in male mice. Activity tagging revealed that cricket hunting activated a subset of glutamatergic neurons in the superior colliculus (SC). Selective stimulation of these hunting-activated neurons alleviated chronic hyperalgesia, primarily mediated by their projections to the zona incerta (ZI). Notably, repeated engagement, either through the hunting paradigm or by repeatedly activating hunting-activated SC-ZI projections, induced sustained analgesia (lasting at least 6 hours), linked to potentiated glutamatergic inputs to ZI GABAergic neurons. Furthermore, SC-ZI projections originating from SC neurons expressing tachykinin precursor 1 (Tac1) selectively elevated neuropathic pain thresholds via substance P release and neurokinin 1 (NK1) receptor-dependent excitatory synaptic transmission onto ZI GABAergic neurons. Together, we show that a specific SC-ZI circuit drives attention-induced analgesia, highlighting the SCTac1-ZI pathway as a therapeutic target for chronic pain.