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Alcohol is thought to exert its effect by acting on gamma-aminobutyric (GABA) inhibitory neurotransmission. The N100, the negative peak on electroencephalography (EEG) that occurs approximately 100 ms following the transcranial magnetic stimulation (TMS) pulse, is believed to represent GABA B  receptor mediated neurotransmission. However, no studies have examined the effect of alcohol on the N100 response to TMS stimulation of the dorsolateral prefrontal cortex (DLPFC). In the present study, we aimed to explore the effect of alcohol on the DLPFC TMS-evoked N100 response. The study was a within-subject cross-over design study. Fifteen healthy alcohol drinkers were administered TMS to the DLPFC before (PreBev) and after consumption (PostBev) of an alcohol or placebo beverage. The amplitude of the N100 before and after beverage was compared for both the alcohol and placebo beverage. Alcohol produced a significant decrease in N100 amplitude (t = 4.316, df = 14, p = 0.001). The placebo beverage had no effect on the N100 amplitude (t = −1.856, df = 14, p = 0.085). Acute alcohol consumption produces a decrease in N100 amplitude to TMS stimulation of the DLPFC, suggesting a decrease in GABA B  receptor mediated neurotransmission. Findings suggest that the N100 may represent a marker of alcohol’s effects on inhibitory neurotransmission.

Alcohol Impairs N100 Response to Dorsolateral Prefrontal Cortex Stimulation