Social defeat is induced by physical and psychological stresses, and implicates the cerebral cortex and multiple brain regions of the limbic system [6–8]. Among these regions, the basolateral amygdala (BLA) establishes and consolidates conditioned fears and harmful stimulations. The establishment of conditioned defeat is impaired by infusing the BLA with anisomycin to inhibit protein synthesis. The consolidation of conditioned defeat is enhanced by overexpressing the cyclic adenosine monophosphate (cAMP) response element binding protein in the BLA through a viral vector [9–11]. Therefore, fear consolidation involves a new type of protein synthesis and the formation of neural microcircuit in the BLA. The medial prefrontal cortex (mPFC) is associated with the motivation and the integration in the development of depression and autism. On the one hand, stress stimulation inhibits the mPFC. On the other hand, mPFC activity caused by optogenetics or deep brain stimulation alleviates the symptoms of depression, and which partially contributes to fear extinction through unclear mechanisms [12, 13]. The hippocampus plays pivotal roles in regulating social behavior. Significant evidence indicates that the dorsal and ventral hippocampus (vHIP) play different roles in processing fear and harmful information from context and conditional stimulation . The bidirectional neural circuit between the vHIP and the hypothalamus integrates harmful information and then determines the vulnerability or resilience toward stress stimulation .