COMT polymorphism modulates the resting‐state EEG alpha oscillatory response to acute nicotine in male non‐smokers |
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| Authors: | H Bowers D Smith S de la Salle J Choueiry D Impey T Philippe H Dort A Millar M Daigle P R Albert A Beaudoin V Knott |
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| Institution: | 1. Department of Psychology, University of Guelph, Guelph, ON, Canada;2. Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada;3. School of Psychology, University of Ottawa, Ottawa, ON, Canada;4. University of Ottawa Institute of Mental Health Research, Royal Ottawa Mental Health Care Centre, Ottawa, ON, Canada;5. Ottawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada |
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| Abstract: | Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists, and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neurotransmission. As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol‐O‐methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting‐state electroencephalographic (EEG) oscillations. In a sample of 62 healthy non‐smoking adult males, a single dose (6 mg) of nicotine gum administered in a randomized, double‐blind, placebo‐controlled design was shown to affect α oscillatory activity, increasing power of upper α oscillations in frontocentral regions of Met/Met homozygotes and in parietal/occipital regions of Val/Met heterozygotes. Peak α frequency was also found to be faster with nicotine (vs. placebo) treatment in Val/Met heterozygotes, who exhibited a slower α frequency compared to Val/Val homozygotes. The data tentatively suggest that interindividual differences in brain α oscillations and their response to nicotinic agonist treatment are influenced by genetic mechanisms involving COMT. |
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| Keywords: | Alpha catechol‐O‐methyltransferase cognition dopamine electroencephalography genotype nicotine oscillations polymorphism resting state |
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