Acute stress relates to high prevalence of anxiety, depression or even sudden death. Although dopaminergic system in amygdala-medial prefrontal cortex (mPFC) circuit is hyper-responsive to stress-induced anxiety, the mechanisms that control anxiety still remains unanswered. Here, the acute restraint stress model(ARS) was established to develop anxiety-like behavior. The D2-dopamine receptor (D2R) availability in amygdala and mPFC was assessed using 18F]-fallypride positron emission tomography(PET) and immunohistochemical assay. We revealed that ARS paradigm was successfully established, as evidenced by elevated plus-maze test(EPM) and increased corticosterone release. Moreover, PET imaging displayed elevated D2R availability in the amygdala and mPFC in ARS as compared to that in the naives. PET imaging combined with immunohistochemical assay confirmed that amygdaloid D2R was significantly implicated in stress-induced anxiety. Our findings delivered valuable insights into neuromechanism of amygdaloid D2R underlying stress-induced anxiety and might have important implications for developing therapeutics for anxiety by targeting amygdaloid D2R. Schematic illustration of the proposed model depicting how enhanced D2R is implicated in ARS-induced anxiety. The amygdala is under a powerful inhibitory control of mPFC in anxiety. D2R tends to play a role in setting up adaptive responses under stressors. The augmented D2R activity in amygdala-mPFC circuit might trigger a crosstalk between amygdala and mPFC that thought to diminish the anxiogenic output of amygdala by initiating a rewarding effects. [Display omitted] • Anxiety-like behaviour was elicited by the acute restraint stress model(ARS) in rats. • PET imaging reveals enhanced D2R expression in amygdala and mPFC in ARS-induced anxiety. • Amygdaloid D2R was significantly implicated in stress-induced anxiety. • Augmented D2R activity triggers a crosstalk between amygdala and mPFC that diminishes the anxiogenic output of amygdala. [ABSTRACT FROM AUTHOR]