ArticlePsychopharmacology2016
Tobacco use is associated with reduced amplitude and intensity dependence of the cortical auditory evoked N1-P2 component.
Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Enhancing precision in human neuroscience.eLife · 2023Review
- The Big Five Personality Traits and Brain Arousal in the Resting State.Brain sciences · 2021Article
- Tobacco and Nervous System Development and Function-New Findings 2015-2020.Brain sciences · 2021Review
- Examining differences in attentional bias to smoking-related cues among black and white cigarette smokers: An event-related potential pilot study.Neuroscience letters · 2020Article
- Biomarkers and neuromodulation techniques in substance use disorders.Bioelectronic medicine · 2020Review
- Human brain arousal in the resting state: a genome-wide association study.Molecular psychiatry · 2019Article
- Evoked potentials and behavioral performance during different states of brain arousal.BMC neuroscience · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleTobacco use is linked to cerebral atrophy and reduced cognitive performance in later life. However, smoking-related long-term effects on brain function remain largely uncertain. Previous studies suggest that nicotine affects serotonergic signaling, and the intensity dependence (alias loudness dependence) of the auditory evoked N1-P2 potential has been proposed as a marker of serotonergic neurotransmission.
objectiveIn the present study, we assesed the effects of chronic smoking on amplitude and intensity dependence of the auditory evoked N1-P2 potential.
methodsSubjects underwent a 15-min intensity dependence of auditory evoked potentials (IAEP) paradigm. From N = 1739 eligible subjects (40-79 years), we systematically matched current smokers, ex-smokers, and never-smokers by sex, age, alcohol and caffeine consumption, and socioeconomic status. Between-group differences and potential dose-dependencies were evaluated.
resultsAnalyses revealed higher N1-P2 amplitudes and intensity dependencies in never-smokers relative to ex- and current smokers, with ex-smokers exhibiting intermediate intensity dependencies. Moreover, we observed pack years and number of cigarettes consumed per day to be inversely correlated with amplitudes in current smokers.
conclusionsAccording to the IAEP serotonin hypothesis, our results suggest serotonin activity to be highest in current smokers, intermediate in ex-smokers, and lowest in never-smokers. To our knowledge, the present study is the first providing evidence for a dose-dependent reduction in N1-P2 amplitudes. Further, we extend prior research by showing reduced amplitudes and intensity dependencies in ex-smokers even 25 years, on average, after cessation. While we can rule out several smoking-related confounders to bias observed associations, causal inferences remain to be established by future longitudinal studies.
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