PMID- 29705707 OWN - NLM STAT- MEDLINE DCOM- 20191101 LR - 20191210 IS - 1873-6823 (Electronic) IS - 0741-8329 (Print) IS - 0741-8329 (Linking) VI - 70 DP - 2018 Aug TI - Alcohol affects the P3 component of an adaptive stop signal task ERP. PG - 1-10 LID - S0741-8329(17)30808-X [pii] LID - 10.1016/j.alcohol.2017.08.012 [doi] AB - 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. CI - Copyright (c) 2017 Elsevier Inc. All rights reserved. FAU - Plawecki, Martin H AU - Plawecki MH AD - Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, United States. Electronic address: mplaweck@iupui.edu. FAU - Windisch, Kyle A AU - Windisch KA AD - Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, United States; The Laboratory of the Biology of Addictive Diseases, The Rockefeller University, New York, NY, United States. FAU - Wetherill, Leah AU - Wetherill L AD - Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, United States. FAU - Kosobud, Ann E K AU - Kosobud AEK AD - Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, United States. FAU - Dzemidzic, Mario AU - Dzemidzic M AD - Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, United States. FAU - Kareken, David A AU - Kareken DA AD - Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, United States. FAU - O'Connor, Sean J AU - O'Connor SJ AD - Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, United States; R.L. Roudebush Veterans Administration Medical Center, Indianapolis, IN, United States. LA - eng GR - TL1 TR001107/TR/NCATS NIH HHS/United States GR - UL1 TR001108/TR/NCATS NIH HHS/United States GR - C06 RR020128/RR/NCRR NIH HHS/United States GR - P60 AA007611/AA/NIAAA NIH HHS/United States GR - UL1 TR000006/TR/NCATS NIH HHS/United States PT - Controlled Clinical Trial PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't DEP - 20170831 PL - United States TA - Alcohol JT - Alcohol (Fayetteville, N.Y.) JID - 8502311 RN - 3K9958V90M (Ethanol) SB - IM MH - Adult MH - Ethanol/*pharmacology MH - Event-Related Potentials, P300/*drug effects/physiology MH - Female MH - Humans MH - *Inhibition, Psychological MH - Male MH - Psychomotor Performance/drug effects/physiology MH - Single-Blind Method MH - Young Adult PMC - PMC5932288 MID - NIHMS902898 OTO - NOTNLM OT - Alcohol OT - Event-related potential (ERP) OT - P300 OT - Response inhibition OT - Response strategy EDAT- 2018/05/01 06:00 MHDA- 2019/11/02 06:00 PMCR- 2019/08/01 CRDT- 2018/04/30 06:00 PHST- 2017/06/23 00:00 [received] PHST- 2017/08/22 00:00 [revised] PHST- 2017/08/24 00:00 [accepted] PHST- 2018/05/01 06:00 [pubmed] PHST- 2019/11/02 06:00 [medline] PHST- 2018/04/30 06:00 [entrez] PHST- 2019/08/01 00:00 [pmc-release] AID - S0741-8329(17)30808-X [pii] AID - 10.1016/j.alcohol.2017.08.012 [doi] PST - ppublish SO - Alcohol. 2018 Aug;70:1-10. doi: 10.1016/j.alcohol.2017.08.012. Epub 2017 Aug 31.