Uncovering the neurobiological processes underlying substance use disorder informs future therapeutic interventions. Prior research implicates the corticotropin releasing factor (CRF) system as a major player in a wide variety of substance use disorder -like phenotypes. However, the complexity of the CRF system in regard to brain region specific effects and experience-dependent changes in activity is poorly understood. Employing a cocaine self-administration paradigm that induces escalation of cocaine consumption in a subset of subjects, we investigated the role of CRF activity in the Nucleus Accumbens (NAc) in cocaine-taking patterns both before and after chronic cocaine experience. Our results showed that pharmacologically inhibiting CRF-R1 in the NAc did not reduce cocaine consumption following escalation and genetically deleting CRF-R1 from cells in the NAc did not prevent escalation. Overall, this suggests that any effect of CRF activity driving escalation or high levels of cocaine consumption is not through its actions on CRF-R1 in the NAc.