The decision to interact with or avoid another individual is fundamental for the survival of many species. Indeed, while affiliative (reward) interactions with conspecific predispose approach behaviors, antagonist (aggressive/defensive) contacts endorse avoidance. Here we use mice to ask how the brain encodes the valence assignment to social stimuli. We demonstrated that dopamine receptor D1-expressing medium spiny neurons (D1-MSNs) in the Nucleus Accumbens (NAc) both respond to prosocial and aggressive social interactions. We found D1-MSN strongly connected with glutamatergic neurons from the Anterior Insular Cortex (AIC) that also express D1Rs. A day after social interaction, we identified dichotomous, long-term valencedependent synaptic plasticity at AIC to LNAc synapses. While prosocial contacts change the ratio between AMPA and NMDA receptors, aggressive interactions drive the insertion of AMPARs lacking the GluA2 subunit. Finally, using optogenetic tools, we linked specific neuronal activity to social valence-dependent plasticity and found that these form of plasticity at AIC to LNAc synapses instructs learned approach and avoidance behavior. In conclusions, by recruiting the same D1R positives neurons within AIC-NAc circuit, we demonstrated a long-term synaptic plasticity that is a signature of social valence and can be tuned by the firing frequency.