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<p>The medial prefrontal cortex (mPFC), a critical hub for social regulation, is highly vulnerable to stress. While mPFC dysfunction underlies stress-induced social alterations, the precise circuit mechanisms underlying remain elusive. Given mPFC’s integration of stress signals from key nodes like the basolateral amygdala (BLA) and paraventricular hypothalamus (PVN), we hypothesized that enhanced BLA and PVN inputs disrupts mPFC’s circuit dynamics, mediating social alterations after stress exposure. Here, using longitudinal in vivo Ca²⁺ imaging during repeated restraint stress, we observed post-stress mPFC hypoactivity, impaired pattern decorrelation and disrupted population coding for social discrimination following both acute and chronic stress. Further combining circuit-specific optogenetics, we revealed that the mPFC dysfunction arise from convergent potentiation of dual inhibitory circuits, including the BLA glutamatergic inputs activating GABAergic neurons and the PVN oxytocinergic projections activating OXTR⁺ GABAergic interneurons. Critically, suppressing either circuit rescued mPFC hypoactivity, restored its encoding for social discrimination, and normalized social performance in stressed mice. Together, these findings establish a unified circuit pathology wherein BLA and PVN hyperactivity converts environmental stress into social alterations, by disrupting the downstream mPFC’s activity dynamics, coactivity pattern, and population coding essential for social discrimination.</p>

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Medial prefrontal cortex neurons integrate amygdala and hypothalamic oxytocin signals to mediate stress-induced social alterations

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月23日

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  • Yujing Zhang,
  • Zi-Qi Zhang,
  • Zi-Jie Zhai,
  • Xuchao Ren,
  • Siyi Zuo,
  • Zheng Ma,
  • Min Liu,
  • Dong Li,
  • Yue Wang,
  • Pan Xu

摘要

The medial prefrontal cortex (mPFC), a critical hub for social regulation, is highly vulnerable to stress. While mPFC dysfunction underlies stress-induced social alterations, the precise circuit mechanisms underlying remain elusive. Given mPFC’s integration of stress signals from key nodes like the basolateral amygdala (BLA) and paraventricular hypothalamus (PVN), we hypothesized that enhanced BLA and PVN inputs disrupts mPFC’s circuit dynamics, mediating social alterations after stress exposure. Here, using longitudinal in vivo Ca²⁺ imaging during repeated restraint stress, we observed post-stress mPFC hypoactivity, impaired pattern decorrelation and disrupted population coding for social discrimination following both acute and chronic stress. Further combining circuit-specific optogenetics, we revealed that the mPFC dysfunction arise from convergent potentiation of dual inhibitory circuits, including the BLA glutamatergic inputs activating GABAergic neurons and the PVN oxytocinergic projections activating OXTR⁺ GABAergic interneurons. Critically, suppressing either circuit rescued mPFC hypoactivity, restored its encoding for social discrimination, and normalized social performance in stressed mice. Together, these findings establish a unified circuit pathology wherein BLA and PVN hyperactivity converts environmental stress into social alterations, by disrupting the downstream mPFC’s activity dynamics, coactivity pattern, and population coding essential for social discrimination.