To determine if overnight tobacco abstinent carriers of the AG or GG (*G) vs. the AA variant of the human mu opioid receptor (OPRM1) A118G polymorphism (rs1799971) differ in [11C]carfentanil binding after tobacco smoking.Methods:
Twenty healthy American male smokers who abstained from tobacco overnight were genotyped and completed positron emission tomography (PET) scans with the mu opioid receptor agonist, [11C]carfentanil. They smoked deniconized (denic) and average nicotine (avnic) cigarettes during the PET scans.Results:
Smoking avnic cigarette decreased the binding potential (BPND) of [11C]carfentanil in the right medial prefrontal cortex (mPfc; 6, 56, 18), left anterior medial prefrontal cortex (amPfc; − 2, 46, 44), right ventral striatum (vStr; 16, 3, − 10), left insula (Ins; − 42, 10, − 12), right hippocampus (Hippo; 18, − 6, − 14) and left cerebellum (Cbl; − 10, − 88, − 34), and increased the BPND in left amygdala (Amy; − 20, 0, − 22), left putamen (Put; − 22, 10, − 6) and left nucleus accumbens (NAcc; − 10, 12, − 8). In the AA allele carriers, avnic cigarette smoking significantly changed the BPND compared to after denic smoking in most brain areas listed above. However in the *G carriers the significant BPND changes were confirmed in only amPfc and vStr. Free mu opioid receptor availability was significantly less in the *G than the AA carriers in the Amy and NAcc.Conclusion:
The present study demonstrates that BPND changes induced by avnic smoking in OPRM1 *G carriers were blunted compared to the AA carriers. Also *G smokers had less free mu opioid receptor availability in Amy and NAcc.