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<p>Empathy, ranging from emotional contagion to consolation, is central to social cognition. While neural mechanisms of observed pain are well studied, how witnessing trauma affects empathy-related behaviors remains unclear. Using an observational social defeat (OSD) model, we find that OSD-exposed mice display enhanced allogrooming toward defeated conspecifics, indicating increased consolation behavior. Whole-brain cFos mapping and fiber photometry reveal selective activation of medial amygdala (MeA) GABAergic neurons during empathic allogrooming. NG2 glia modulate this behavior via GABA signaling; their specific ablation in the MeA reduces inhibitory synaptic transmission, disinhibiting neighboring GABAergic neurons and increasing allogrooming. Single-cell RNA analysis reveals that GABA signaling originates from <i>Gad1</i>-expressing NG2 glia. Genetic knockout of <i>Gad1</i> in NG2 glia recapitulates the phenotype. This mechanism requires elevated corticosterone induced by social defeat. Our findings highlight the role of NG2 glia-GABA neuron interactions in promoting prosocial empathy and suggest targeting GABA signaling in NG2 glia as a potential therapeutic strategy for vicarious trauma.</p>

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GABA signaling in NG2 glia mediates empathy-like behavior under observational social defeat

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月25日

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  • Yujin Jian,
  • Shengyu Jin,
  • Peng Liu,
  • Xiaoli Zheng,
  • Xiaoqi Hong,
  • Yong Han,
  • Alexey Semyanov,
  • Shumin Duan,
  • Xiaoping Tong

摘要

Empathy, ranging from emotional contagion to consolation, is central to social cognition. While neural mechanisms of observed pain are well studied, how witnessing trauma affects empathy-related behaviors remains unclear. Using an observational social defeat (OSD) model, we find that OSD-exposed mice display enhanced allogrooming toward defeated conspecifics, indicating increased consolation behavior. Whole-brain cFos mapping and fiber photometry reveal selective activation of medial amygdala (MeA) GABAergic neurons during empathic allogrooming. NG2 glia modulate this behavior via GABA signaling; their specific ablation in the MeA reduces inhibitory synaptic transmission, disinhibiting neighboring GABAergic neurons and increasing allogrooming. Single-cell RNA analysis reveals that GABA signaling originates from Gad1-expressing NG2 glia. Genetic knockout of Gad1 in NG2 glia recapitulates the phenotype. This mechanism requires elevated corticosterone induced by social defeat. Our findings highlight the role of NG2 glia-GABA neuron interactions in promoting prosocial empathy and suggest targeting GABA signaling in NG2 glia as a potential therapeutic strategy for vicarious trauma.