Alcohol affects the P3 component of an adaptive stop signal task ERP

Abstract

Background: The P3 component of the event-related potential (ERP) has been particularly useful in alcohol research for identifying endophenotypes of alcohol-use disorder (AUD) risk in sober subjects. However, practice and/or fatigue reduce P3 amplitude, limiting the ability to ascertain acute and adaptive effects of alcohol exposure. Here, we report acute alcohol effects on P3 amplitude and latency using an adaptive stop signal task (aSST).

Methods: One hundred forty-eight non-dependent moderate to heavy social drinkers, ages 21 to 27, participated in two single-blind, alcohol or placebo, counterbalanced sessions approximately 1 week apart. During each session, subjects performed an adaptive stop signal task (aSST) at 1) baseline, 2) upon reaching the target 60 mg/dL breath alcohol concentration or at the equivalent time during the placebo session, and 3) approximately 135 min later while the breath alcohol concentration was clamped. Here, we report on differences between baseline and first subsequent measurements across the experimental sessions. During each aSST run, the stop signal delay (SSD, the time between stop and go signals) adjusted trial-by-trial, based on the subject's performance.

Results: The aSST reliably generated a STOP P3 component that did not change significantly with repeated task performance. The pre-infusion SSD distribution was bimodal, with mean values several hundred msec apart (FAST: 153 msec and SLOW: 390 msec). This suggested different response strategies: FAST SSD favoring "going" over "stopping", and SLOW SSD favoring "stopping" over "going". Exposure to alcohol at 60 mg/dL differentially affected the amplitude and latency of the STOP P3 according to SSD group. Alcohol significantly reduced P3 amplitude in the SLOW SSD compared to the FAST SSD group, but significantly increased P3 latency in the FAST SSD compared to the SLOW SSD group.

Conclusions: The aSST is a robust and sensitive task for detecting alcohol-induced changes in inhibition behavior as measured by the P3 component in a within-subject design. Alcohol was associated with P3 component changes, which varied by SSD group, suggesting a differential effect as a function of task strategy. Overall, the data support the potential utility of the aSST in the detection of alcohol response-related AUD risk.

Keywords: Alcohol; Event-related potential (ERP); P300; Response inhibition; Response strategy.

Copyright © 2017 Elsevier Inc. All rights reserved.

Figures

Fig. 1

Experimental Design. Adaptive Stop Signal Task (aSST) was performed in two consecutive runs (4.5 min/run), in a fixed order with other dependent measures, and began approximately 17 minutes within each of three 45 minute blocks during the infusion sessions. Sub-block aSST assessments were analyzed together. Block 0, or Baseline, occurred before infusion of either alcohol or placebo. Block 1 was collected beginning 20 minutes after the initiation of alcohol/placebo infusion and Block 2 initiated 90 minutes after the completion of Block 1. Sessions were scheduled nominally 7 days apart.

Fig. 2

Comparison of Session 1 Baseline Stop Signal Delay Density and 2 Component Gaussian Mixture Model.

Fig. 3

Baseline Grand Mean STOP ERPs. Grand Mean STOP ERPs at electrode locations Fz (Top), Cz (Middle), and Pz (Bottom) are displayed for each of the 3 SSD groups for Baseline Session 1 (Left) and Session 2 (Right). Each waveform reflects application of the modified ADJAR decontamination procedure.

Fig. 4

Baseline P3 Amplitude and Latency by Session and SSD group. P3 Amplitude (Left, Closed Bars): No baseline P3 amplitude differences between FAST and SLOW SSD groups was observed across sessions. SLOW SSD group baseline P3 amplitude was significantly reduced in Session 2 versus Session 1. P3 Latency (Right, Open Bars): FAST SSD group baseline P3 latency was significantly longer than that of SLOW SSD group across sessions. FAST SSD group baseline P3 latency was significantly reduced in Session 2 versus Session 1. (* p

Fig. 5

Differences of Grand Mean STOP ERPs. Tempero-spatial differences between FAST and SLOW SSD groups in the initial responses to placebo administration (IRP), initial responses to alcohol exposure at 60mg/dL (IRA), and the alcohol effect (AE) calcualted as the difference of differences (IRA-IRP)are displayed. None of these signals were actually measured and the comparison is meant only to illustrate group effects observed in association with alcohol exposure.

Fig. 6

Effect of Alcohol on STOP P3 Amplitude and Latency. Alcohol significantly decreased |P3| for SLOW SSD compared to FAST SSD group (a). Alcohol significantly lengthened P3 latency for FAST SSD compared to SLOW SSD group (b). (* p