Early-life adversity (ELA) is a leading risk factor for developing mental disorders such as depression or anxiety in adulthood. Some of its anatomical and molecular correlates were described under multiple stress paradigms, acute and chronic alike, in various species. However it is unclear how the cellular substrate of traumatic memories associated with ELA evolves through life and can participate in its behavioral outcome. To allow lifelong tracking of neuronal populations recruited during early-life stress we used FosTRAP2 mice in a juvenile (P21) social defeat model (jSD), in which neuronal activation results in the irreversible expression of the fluorescent reporter TdTomato in neurons activated during a defined temporal window. This design aims at assessing brain-wide neuronal ensembles activated during the experience of jSD, and reactivated at different timepoints in a social interaction context. TdTomato was allowed to be expressed on the last day of aggression (P28), and the re-activation of tagged neurons was assessed by c-fos immunohistochemistry after a social interaction test in three different cohorts, at P42, P77 and P105 respectively.Our results highlight that SDj induces a strong social aversion, that is maintained through adulthood but with different temporal dynamics in male and female mice, which show different patterns of susceptibility and resilience. Further analysis are ongoing to investigate how changes in the behavioral outcome of jSD over-time correlates with temporal changes in cellular reactivation and will be aimed at identifying how manipulating the activity of these neuronal populations can mitigate the long lasting impact of ELA.