Post-traumatic stress disorder (PTSD) emerges in the aftermath of a traumatic event, underscoring the pressing need for research into preventive treatments. Adrenal glucocorticoids induce short-term physiological adaptations necessary to cope with the threat. Evidence indicates that when administrated after trauma, glucocorticoids prevent the development of PTSD. The basolateral amygdala (BLA) is a key structure for processing positive and negative valence which communicates bidirectionally with other regions to regulate the stress responses. The present study evaluates the efficacy of corticosterone as a preventive treatment for a PTSD-like immobilization (IMO) animal model and to discern the role of BLA neurons in this stress paradigm. Here, we combine behavioral assessment with in vivo deep-brain calcium imaging (Miniscopes) in freely moving mice. Moreover, corticosterone can prevent the deficit in social motivation and anxiety-like behavior induced by IMO during the social interaction test and elevated plus maze. Results show lower neuronal BLA reactivation in mice treated with corticosterone when evaluating anxiety and depressive-like behavior. Also, we identify neuronal responses (excited, inhibited, unresponsive) during the behavioral tests depending on whether the mice were treated with corticosterone or vehicle. In brief, our results reveal how neural signals in the BLA evolve during the stress model and how corticosterone can alter the behavioral phenotype and neural activity.