The p300 brain potential is reduced in smokers

A. P. Anokhin; A. B. Vedeniapin; E. J. Sirevaag; L. O. Bauer; S. J. O'Connor; S. Kuperman; B. Porjesz; T. Reich; H. Begleiter; J. Polich; J. W. Rohrbaugh

doi:10.1007/s002130000387

The p300 brain potential is reduced in smokers

A. P. Anokhin, A. B. Vedeniapin, E. J. Sirevaag, L. O. Bauer, S. J. O'Connor, S. Kuperman, B. Porjesz, T. Reich, H. Begleiter, J. Polich, J. W. Rohrbaugh

Research output: Contribution to journal › Article › peer-review

86 Scopus citations

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. Exsmokers 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.

Original language	English
Pages (from-to)	409-413
Number of pages	5
Journal	Psychopharmacology
Volume	149
Issue number	4
DOIs	https://doi.org/10.1007/s002130000387
State	Published - 2000

Keywords

ERPs
Nicotine. Addiction
P300
Smoking

Access to Document

10.1007/s002130000387

Cite this

@article{5aa5fb6363fb473dbc07c3f2212e1b7e,

title = "The p300 brain potential is reduced in smokers",

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. Exsmokers 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.",

keywords = "ERPs, Nicotine. Addiction, P300, Smoking",

author = "Anokhin, {A. P.} and Vedeniapin, {A. B.} and Sirevaag, {E. J.} and Bauer, {L. O.} and O'Connor, {S. J.} and S. Kuperman and B. Porjesz and T. Reich and H. Begleiter and J. Polich and Rohrbaugh, {J. W.}",

note = "Funding Information: Acknowledgements The Collaborative Study on the Genetics of Alcoholism (H. Begleiter, SUNY HSCB, Principal Investigator, T. Reich, Washington University, Co-Principal Investigator) includes six different centers where data collection takes place. The six sites and Principal Investigators and Co-Investigators are: Indiana University (J. Nurnberger Jr, T.-K. Li, P. M. Conneally, H. Edenberg); University of Iowa (R. Crowe, S. Kuperman); University of California, San Diego and The Scripps Research Institute (M. Schuckit, F. Bloom); University of Connecticut (V. Hessel-brock); State University of New York, Health Sciences Center (H. Begleiter, B. Porjesz); Washington University in St Louis (T. Reich, C. R. Cloninger, J. Rice). Supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) by USPHS grants NIAAA U10AA08401, U10AA08402 and U10AA08403. A. A. was supported by an institutional post-doctoral training grant from the National Institute of Drug Abuse, DA07261.",

year = "2000",

doi = "10.1007/s002130000387",

language = "English",

volume = "149",

pages = "409--413",

journal = "Psychopharmacology",

issn = "0033-3158",

number = "4",

}

TY - JOUR

T1 - The p300 brain potential is reduced in smokers

AU - Anokhin, A. P.

AU - Vedeniapin, A. B.

AU - Sirevaag, E. J.

AU - Bauer, L. O.

AU - O'Connor, S. J.

AU - Kuperman, S.

AU - Porjesz, B.

AU - Reich, T.

AU - Begleiter, H.

AU - Polich, J.

AU - Rohrbaugh, J. W.

N1 - Funding Information: Acknowledgements The Collaborative Study on the Genetics of Alcoholism (H. Begleiter, SUNY HSCB, Principal Investigator, T. Reich, Washington University, Co-Principal Investigator) includes six different centers where data collection takes place. The six sites and Principal Investigators and Co-Investigators are: Indiana University (J. Nurnberger Jr, T.-K. Li, P. M. Conneally, H. Edenberg); University of Iowa (R. Crowe, S. Kuperman); University of California, San Diego and The Scripps Research Institute (M. Schuckit, F. Bloom); University of Connecticut (V. Hessel-brock); State University of New York, Health Sciences Center (H. Begleiter, B. Porjesz); Washington University in St Louis (T. Reich, C. R. Cloninger, J. Rice). Supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) by USPHS grants NIAAA U10AA08401, U10AA08402 and U10AA08403. A. A. was supported by an institutional post-doctoral training grant from the National Institute of Drug Abuse, DA07261.

PY - 2000

Y1 - 2000

N2 - 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. Exsmokers 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.

AB - 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. Exsmokers 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.

KW - ERPs

KW - Nicotine. Addiction

KW - P300

KW - Smoking

UR - http://www.scopus.com/inward/record.url?scp=0034111233&partnerID=8YFLogxK

U2 - 10.1007/s002130000387

DO - 10.1007/s002130000387

M3 - Article

C2 - 10867969

AN - SCOPUS:0034111233

VL - 149

SP - 409

EP - 413

JO - Psychopharmacology

JF - Psychopharmacology

SN - 0033-3158

IS - 4

ER -

The p300 brain potential is reduced in smokers

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this