Introduction to the study: Tobacco smoking is the main cause of preventable death worldwide with about 5 million deaths each year. Nicotine is the principal addictive component of tobacco smoke and works in the brain by interaction with the nicotinic acetylcholine receptors. The α4β2 nicotinic acetylcholine receptor has a special relevance because it triggers an increased dopamine release in the nucleus accumbens after nicotine intake, thereby modulating the reward system. Many studies have shown a genetic determination of nicotine dependence and an association between genetic variants of certain nicotinic acetylcholine receptors (e.g. the CHRNA4 SNP rs1044396) and nicotine dependence.
The event-related EEG-potential P300 is a marker for cortical function. A reduction of the P300 amplitude was shown for smokers and for people with other psychiatric disorders.
In this study we aimed to reproduce the P300 amplitude reduction as it was demonstrated in previous studies and we also wanted to investigate a possible role of the genetic variants of the CHRNA4 SNP rs1044396.
Methods: 277 healthy subjects, 156 non-smokers and 121 smokers, were investigated by measuring the P300 and by analyzing the genotype of SNP rs1044396.
Results: A significant P300 amplitude reduction was found in smokers compared to non-smokers independently of cofactors age and gender (Fz: p=0,040; Pz: p<0,001). We also found an increased P300 amplitude reduction when subjects were compared regarding the number of cigarettes smoked per day and the pack years (p=0,019 und p=0,001), but this effects was no longer significant after correction for age and gender. The investigated influence of the genotype of CHRNA4 SNP rs1044396 on the smoking status did not shown a significant effect (p=0,208). Finally, there was no significant association between the SNP rs1044396 genotype and the P300 amplitude, and this did not change when data regarding smoking status was included.
Conclusion: The results of this study reaffirm previous findings that the P300 amplitude and the level of nicotine consumption are inversely correlated. The expected association between the SNP rs1044396 genotype and smoking status or P300 amplitude reduction was not found, however. Therefore, further studies are required to find out if there is a genetic source for the effects of nicotine on the P300 amplitude and which genes or variants are involved.
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