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18 reviewsSUMMARYTransient sensory experiences can trigger sustained emotional disturbances, yet the underlying neuralmechanisms remain unclear. Here, we show that acute pain induces persistent anxiety in male mice, independent of ongoing nociceptive input, through reduced oxytocin signaling in the dorsal bed nucleus ofthe stria terminalis (dBNST). Reactivating oxytocin receptors (Oxtrs) in the dBNST markedly alleviatedanxiety-like behaviors following pain resolution. Mechanistically, chemogenetic inhibition of somatostatinexpressing (SST) neurons in the dBNST (dBNSTSST neurons) abolished oxytocin’s anxiolytic effects, whilepharmacological blockade or selective knockdown of Oxtrs in these neurons increased anxiety-like behaviors. Transcriptomic and electrophysiological analyses further revealed that alterations in synaptic transmission and intrinsic excitability participate in this anxiety state. Together, these findings define a multilevelframework—spanning molecular, cellular, and circuit mechanisms—by which acute sensory input induceslong-term emotional dysregulation. This study advances our understanding of pain-related affective disorders and highlights oxytocin signaling and dBNSTSST neurons as promising therapeutic targets.