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Abstract
Background: Priming doses of alcohol are associated with increased desire to drink and disinhibitory effects on subsequent control over drinking. Despite the importance of alcohol priming in the cue-reactivity literature, the effects of priming on brain responses to alcohol cues remains unclear. Furthermore, evidence suggests this relationship may be moderated by OPRM1 genotype. Methods: Twenty individuals with alcohol dependence (six females; 90% Caucasian; mean age = 29.4) who were prospectively genotyped on the OPRM1 gene underwent two functional magnetic resonance imaging (fMRI) sessions, before and after a priming dose of alcohol, each including a gustatory alcohol cue reactivity paradigm and self-reported craving measures. Results: Self-reported alcohol craving generally increased and remained higher for alcohol versus water cue presentations across pre- and post-priming scans. Compared to alcohol cues delivered during the post-priming scan, alcohol cues delivered pre-priming were associated with greater activation in regions including the hippocampus, amygdala, inferior frontal gyrus, temporal cortex, and occipital cortex. Controlling for alcoholism severity increased statistical significance of activation in these regions. Follow-up analyses revealed a positive correlation between alcoholism severity and pre- versus post-priming alcohol cue-reactivity primarily in frontal regions. OPRM1 genotype was also found to moderate alcohol cue-reactivity across scans. Conclusion: This study provides initial evidence of alcohol cue-elicited habituation in fronto-temporal regions, despite continued craving, following a priming dose of alcohol. Further, it provides preliminary evidence for moderating roles of alcoholism severity and OPRM1 genotype on priming-related changes in cue-reactivity, adding to our understanding of the function of alcohol priming in alcohol dependence.
Acknowledgements
The authors would like to thank Andia Heydari, Pauline Chin, and Ellen Chang for their contribution to data collection and data management for this project.
Funding
This study was supported by a grant from ABMRF, the Foundation for Alcohol Research and a grant from NIAAA (1R03 AA019569). KEC was supported by the UCLA Training Program in Translational Neuroscience of Drug Abuse (T32 DA024635) and a National Research Service Award awarded by NIDA (F31 DA035604).
Declaration of interest
LAR is a paid consultant for GSK. All other authors declare that they have no conflicts of interest. The authors alone are responsible for the content and writing of this paper.
Supplementary material available online
Supplementary Tables S1 and S2
Supplementary Figures S1 and S2.