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<p>Traumatic brain injury often accelerates fracture repair, but the neural circuits linking brain state to bone healing remain unclear. Here we show that, in male mice, a hippocampal–cortical circuit linking the dentate gyrus (DG) and the retrosplenial granular cortex (RSGc) regulates repair after bone injury. Skeletal injury increased activity–associated labeling in both regions. Inhibiting excitatory neurons in the DG or RSGc, or suppressing neuronal populations associated with the DG–RSGc pathway, accelerated repair, whereas activating DG or RSGc excitatory neurons delayed healing. RSGc activation counteracted the pro–healing effect of DG inhibition, supporting DG–RSGc circuit dependence under the tested conditions. Inhibitory circuit manipulations were associated with increased circulating neuropeptide Y, macrophage IDO1 induction at the repair site, and elevated L–kynurenine, which promoted osteogenic differentiation. Pharmacological blockade and rescue experiments support an NPY–IDO1–kynurenine effector arm linking central circuit state to peripheral bone repair.</p>

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A circuit linking dentate gyrus and retrosplenial granular cortex regulates fracture healing in male mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • Wei Zhang,
  • Wei Zhang,
  • Yue Guo,
  • Danni Chen,
  • Xiaowen Jiang,
  • Jingjing Zhang,
  • Erman Chen,
  • Yinfeng Yuan,
  • Wanyi Wu,
  • Yiming Qian,
  • Xiaohua Yu,
  • Yongjie Wang,
  • Weixu Li

摘要

Traumatic brain injury often accelerates fracture repair, but the neural circuits linking brain state to bone healing remain unclear. Here we show that, in male mice, a hippocampal–cortical circuit linking the dentate gyrus (DG) and the retrosplenial granular cortex (RSGc) regulates repair after bone injury. Skeletal injury increased activity–associated labeling in both regions. Inhibiting excitatory neurons in the DG or RSGc, or suppressing neuronal populations associated with the DG–RSGc pathway, accelerated repair, whereas activating DG or RSGc excitatory neurons delayed healing. RSGc activation counteracted the pro–healing effect of DG inhibition, supporting DG–RSGc circuit dependence under the tested conditions. Inhibitory circuit manipulations were associated with increased circulating neuropeptide Y, macrophage IDO1 induction at the repair site, and elevated L–kynurenine, which promoted osteogenic differentiation. Pharmacological blockade and rescue experiments support an NPY–IDO1–kynurenine effector arm linking central circuit state to peripheral bone repair.