We found that social defeat induced by acute aggression is characterized by social fear and avoidance, and is accompanied by a depression-like behavior. Behavioral test revealed that social fear was severe on days 1 and 3 and gradually diminished on days 7 and 15 after aggression. On days 1 and 3 after aggression, the expression of IEGs (including zif268, arc, and c-Fos) increased in the BLA but decreased in the vHIP and mPFC. On days 7 and 15 after aggression, the expression of IEGs decreased in the BLA but increased in the vHIP. Thus, BLA played an important role in establishing social defeat. Equal volumes of Mus and saline were microinjected into the bilateral BLA immediately after aggression to verify this hypothesis. On day 3 after aggression, social fear and freezing behavior were more significantly ameliorated by Mus treatment than by saline treatment. In addition, Mus treatment reduced the expression of IEGs in the BLA but increased that in the vHIP. The amygdala is critical in mediating fear- and anxiety-related behavior and is the key site for the acquisition and storage of fear memory. The plasticity of the sensory inputs from the thalamus and the cortical areas to the projection neurons in the BLA is the core mechanism underlying Pavlovian fear conditioning [23–25]. The associations between conditioned and unconditioned stimuli are formed through this mechanism. According to the neural circuit model of the amygdala function, fear output is generated by the associative information conveyed from the BLA by internuclear excitatory projections from the basal and basomedial nuclei to the medial region of the central amygdala. This passive information transfer model is currently being challenged because growing evidence indicates that the BLA and central amygdala can independently mediate parallel or additional associative functions under aversive conditioning [26, 27]. Another emerging evidence is that fear acquisition is controlled by the plasticity of the inhibitory synapses and the interneurons in the amygdala . On the one hand, regulating the inhibition in the BLA and the specific inhibitory synapses on principal neurons in the BLA is associated with the behavioral suppression of fear following the extinction of learning. On the other hand, the activity of local GABAergic neurons is regulated by the plasticity of their excitatory inputs in the BLA and the central lateral amygdala . A recent study revealed that specific local interneurons in the BLA were differentially recruited during conditioned and un-conditioned stimulation associations, thereby mediating the inhibition and disinhibition of distinct subcellular domains for controlling fear learning. Therefore, multiple plastic systems, particularly those integrating GABAergic neurons, can collectively encode aspects of the stimulus associations in the amygdala. The local interneurons in the BLA are heterogeneous interneurons displaying different morphological, electrophysiological, and neurochemical characteristics. Parvalbumin positive interneurons constitute approximately 40% of these interneurons and exert robust peri-somatic inhibitory effects on the projection neurons [30, 31]. We found that the ratio of c-Fos to parvalbumin double labeled cells in the BLA was approximately 20% of the total c-Fos immunopositive cells on day 3 after social aggression (Additional file 1: Figure S1). These findings suggested that the interneurons in BLA are involved in the regulation of social defeat.