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Description
Spontaneous neural oscillations recorded during wakeful rest are sensitive to a variety of factors including pharmacological manipulations. Research indicates that alcohol intoxication changes these oscillations but the mechanisms underlying interindividual differences in sensitivity to alcohol are poorly understood. A genetic approach can provide insight into neurotransmitter pathways that mediate neural responses to alcohol challenge. Acute alcohol intoxication increases dopamine availability, which plays a key role in cognitive and reward functions. Val158Met is the most studied polymorphism of the COMT gene that regulates cortical dopamine transmission. The aim of this study was to examine the effects of acute alcohol intoxication on spontaneous oscillations as a function of cortical dopamine availability.Healthy young (26.5 ± 4.6 yrs old) social drinkers, who reported no alcohol-related problems participated in four study sessions. They were genotype-stratified into two demographically matched groups of met/met and val/val homozygotes (n = 20 each) characterized by high vs. low dopaminergic tone respectively. Following an introductory session, subjects participated in two beverage sessions in which alcohol and placebo were administered during eyes-open and eyes-closed wakeful rest. Magnetoencephalography (MEG) signals were analyzed with a Fast Fourier transform to calculate power within theta (4 – 7 Hz), alpha (8 – 12 Hz), and beta (15 – 25 Hz) frequency bands in addition to alpha peak frequency (APF). MR images were used to constrain spatial inverse estimates of MEG activity to the cortical surface. Data were analyzed with mixed design ANOVAs. Results revealed that met/met homozygotes had faster APF than val/val carriers which was selectively decreased by alcohol. Overall, closing the eyes increased alpha, theta, and beta power while alcohol increased alpha and beta power. Alcohol-induced slowing of alpha oscillations is observed in high-dopamine met/met homozygotes, providing insight into dopamine-based contributions to these oscillations and their sensitivity to acute alcohol. Acting on dopamine transmission directly and via the mediating effects of GABAergic activity, alcohol slows alpha oscillations by dysregulating thalamocortical networks. These findings could serve as a marker for individual differences in the sensitivity to alcohol and could inform educational and prevention strategies.
