Ethnic group differences in pain perception and prevalence have been well documented. These disparities persist despite controlling for other factors (e.g., sex, socioeconomic status), suggesting differences in endogenous pain modulation. One potential mechanism underlying this disparity might be differences in mu-opioid receptor (MOPR) function, given that MOPRs critically contribute to pain modulation. Previous work demonstrated racial differences in the association between the MOPR gene (OPRM1) and pain perception; however, no study has reported whether differences in MOPR physiology support these genetic findings. The present study sought to address this knowledge gap by examining differences between 24 Black and 26 age-, sex-, education-matched White healthy participants in mu-selective agonist binding (i.e., [ 11 C]-Carfentanil) during a 90-minute dynamic high resolution research tomograph PET imaging session. Participants underwent two counterbalanced scans following application of: 1) 10% capsaicin cream to induce pain and 2) a control cream. Only data from the control scan are presented. Participants also completed a battery of quantitative sensory testing to quantify pain sensitivity outside of the scanner. PET volumes of interest (VOIs) analysis (40 VOIs) demonstrated significant differences between Black and White participant groups in [ 11 C]-Carfentanil binding potential in left dorsolateral prefrontal cortex (dlPFC) and right ventral striatum (vS) VOIs after Bonferroni correction [dlPFC: t48=3.6, p p .001). Results suggest that Black individuals might have greater MOPR availability due to lower MOPR occupancy by endogenous opioids than White peers, with higher binding potential (i.e., lower endogenous opioid binding) associated with greater pain sensitivity across the sample. If replicated, findings have implications for physiological differences underlying ethnicity-related pain disparities, highlighting the need for tailored treatments in historically underserved populations.