Human studies of substance use disorder show that psychological stress and drug availability interact following rehabilitation, contributing to the high relapse potential. Social stressors trigger particularly strong motivation for drug, but how this affects neuronal function to increase relapse is unknown. Animal models, which allow for the dissection of neural mechanisms, primarily utilize physical stressors to trigger relapse. To recapitulate psychosocial post-rehabilitation challenges in animals, we developed a model of social stress-potentiated methamphetamine (METH) seeking. Rats receive a single social defeat (SD) session after completion of self-administration and extinction of lever pressing. While a reminder of the SD was insufficient to reinstate METH seeking on its own, rats that received a reminder of SD followed by a METH-priming injection displayed potentiated reinstatement over METH-priming alone. Examination of neuronal activation patterns of the METH-primed reinstatement session identified c-Fos-immunoreactivity in the basolateral amygdala (BLA) as correlated with SD score, a measure of defeat latency. Rapidly defeated rats showed potentiated METH-primed reinstatement and elevated BLA c-Fos compared with controls. Conversely, rats that were undefeated during the social stress did not show potentiated METH-primed reinstatement or elevated BLA c-Fos. Interestingly, inactivation of the BLA with baclofen/muscimol prior to the stress reminder and METH-priming generated a potentiation of METH seeking in the undefeated rats, suggesting the BLA may mediate resilience to the stressor. This model provides a tool for the further dissection of neural mechanisms mediating social stress-potentiated relapse and for the development of relapse-reducing therapeutics.