Journal article
The P300 brain potential is reduced in smokers
Psychopharmacology, Vol.149(4), pp.409-413
05/2000
DOI: 10.1007/s002130000387
PMID: 10867969
Abstract
Rationale: Tobacco smoking is the most prevalent type of substance abuse, yet its biobehavioral etiology is little understood. Identification of differences between smokers and non-smokers on basic characteristics of neurocognitive functioning may help to elucidate the mechanisms of tobacco dependence. Objectives: This study assessed the relationship between smoking status and the P300 component of event-related potential (ERP) while controlling for potential confounders such as alcoholism, drug abuse, and psychopathology. Methods: The ERP responses elicited by a visual oddball task were measured at the mid-parietal site in 905 current smokers, 463 ex-smokers, and 979 never smokers. Results: P300 amplitude was significantly lower in current cigarette smokers compared to never-smokers. Ex-smokers did not differ significantly from never-smokers. P300 reduction was also associated with alcoholism, drug dependence, and family density of alcoholism. However, after controlling for smoking, only family density of alcoholism remained a significant predictor of P300 amplitude. Conclusions: The results indicate a significant effect of smoking status on P300 amplitude which is additive to family history of alcoholism and suggest that either (1) long-term tobacco smoking may produce a reversible change in brain function, or (2) reduced P300 may be a marker of risk for nicotine dependence.
Details
- Title: Subtitle
- The P300 brain potential is reduced in smokers
- Creators
- A. P Anokhin - Department of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St Louis, MO 63108, USA e-mail: andrey@matlock.wustl.edu, Fax: +1-314-286-2213 USA. B Vedeniapin - Department of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St Louis, MO 63108, USA e-mail: andrey@matlock.wustl.edu, Fax: +1-314-286-2213 USE. J Sirevaag - Department of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St Louis, MO 63108, USA e-mail: andrey@matlock.wustl.edu, Fax: +1-314-286-2213 USL. O Bauer - University of Connecticut School of Medicine, Farmington, Connecticut, USA USS. J O’Connor - Indiana University School of Medicine, Indianapolis, Indiana, USA USS Kuperman - University of Iowa School of Medicine, Iowa City, Iowa, USA USB Porjesz - Department of Psychiatry, Neurodynamics Laboratory, SUNY Health Sciences Center, Brooklyn, New York, New York, USA UST Reich - Department of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St Louis, MO 63108, USA e-mail: andrey@matlock.wustl.edu, Fax: +1-314-286-2213 USH Begleiter - Department of Psychiatry, Neurodynamics Laboratory, SUNY Health Sciences Center, Brooklyn, New York, New York, USA USJ Polich - The Scripps Research Institute, La Jolla, California, USA USJ. W Rohrbaugh - Department of Psychiatry, Washington University School of Medicine, 40 N.Kingshighway, Suite 1, St Louis, MO 63108, USA e-mail: andrey@matlock.wustl.edu, Fax: +1-314-286-2213 US
- Resource Type
- Journal article
- Publication Details
- Psychopharmacology, Vol.149(4), pp.409-413
- Publisher
- Springer-Verlag; Berlin/Heidelberg
- DOI
- 10.1007/s002130000387
- PMID
- 10867969
- ISSN
- 0033-3158
- eISSN
- 1432-2072
- Language
- English
- Date published
- 05/2000
- Academic Unit
- Psychiatry; Stead Family Department of Pediatrics
- Record Identifier
- 9984003428902771
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