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Psychopharmacology (Berl). 2016 Jun;233(11):2173-2183. doi: 10.1007/s00213-016-4268-z. Epub 2016 Mar 17.

Tobacco use is associated with reduced amplitude and intensity dependence of the cortical auditory evoked N1-P2 component.

Author information

1
LIFE - Leipzig Research Center for Civilization Diseases, University of Leipzig, Leipzig, Germany. philippe.jawinski@medizin.uni-leipzig.de.
2
Department of Psychiatry and Psychotherapy, University of Leipzig, Leipzig, Germany. philippe.jawinski@medizin.uni-leipzig.de.
3
Depression Research Center of the German Depression Foundation, Leipzig, Germany. philippe.jawinski@medizin.uni-leipzig.de.
4
LIFE - Leipzig Research Center for Civilization Diseases, University of Leipzig, Leipzig, Germany.
5
Department of Psychiatry and Psychotherapy, University of Leipzig, Leipzig, Germany.
6
Depression Research Center of the German Depression Foundation, Leipzig, Germany.
7
Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig, Germany.

Abstract

RATIONALE:

Tobacco 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.

OBJECTIVE:

In the present study, we assesed the effects of chronic smoking on amplitude and intensity dependence of the auditory evoked N1-P2 potential.

METHODS:

Subjects 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.

RESULTS:

Analyses 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.

CONCLUSIONS:

According 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.

KEYWORDS:

Addiction; Auditory evoked potentials; EEG; Intensity dependence; Loudness dependence; N1-P2; N100; P200; Smoking

PMID:
26983415
DOI:
10.1007/s00213-016-4268-z
[Indexed for MEDLINE]

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