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The medial prefrontal cortex (mPFC), a critical hub for social regulation, is highly vulnerable to stress. While mPFC dysfunction underlies stress-induced social deficits, 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 deficits 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 driving feedforward inhibition 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 deficits, by disrupting the downstream mPFC's activity dynamics, coactivity pattern, and population coding essential for social discrimination.