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JOURNAL ARTICLE
RESEARCH SUPPORT, N.I.H., EXTRAMURAL
RESEARCH SUPPORT, NON-U.S. GOV'T
Nicotine-induced cortical activation among nonsmokers with moderation by trait cognitive control.
Psychopharmacology 2016 June
RATIONALE: Considerable research suggests that nicotine enhances cognitive control-related processes (e.g., attention, memory) among nicotine-deprived smokers, both in terms of behavior and neural indices (e.g., ERP, slow-wave EEG). Nicotine may also increase cognitive control among nonsmokers, and this may vary as a function of trait cognitive control. It is important to examine the effects of nicotine on cognitive control-related processes among nonsmokers as these effects may provide a path for the initiation of smoking.
OBJECTIVES: The objectives of the study were to examine in nonsmokers (1) the effect of nicotine on resting cortical activity, an indirect measure of cognitive control, and (2) trait cognitive control as a moderator of nicotine-induced cortical activity changes.
METHOD: Eighty participants were given placebo and 7-mg nicotine patches in separate sessions for this counter-balanced, double-blind, within-subject study. Resting cortical activity was measured with EEG for a 3-min period with eyes opened.
RESULTS: Average alpha-1 band power density values in frontal and central regions were lower during the nicotine versus placebo condition, which provides evidence of nicotine-induced cortical activation. Furthermore, those with lower self-reported cognitive control exhibited greater nicotine-induced reductions in alpha-1 power density values.
CONCLUSIONS: These individual differences in nicotine-induced cortical activation are consistent with a model of nicotine self-medication whereby individuals with lower cognitive control may find smoking more reinforcing via amelioration of related cognitive deficits.
OBJECTIVES: The objectives of the study were to examine in nonsmokers (1) the effect of nicotine on resting cortical activity, an indirect measure of cognitive control, and (2) trait cognitive control as a moderator of nicotine-induced cortical activity changes.
METHOD: Eighty participants were given placebo and 7-mg nicotine patches in separate sessions for this counter-balanced, double-blind, within-subject study. Resting cortical activity was measured with EEG for a 3-min period with eyes opened.
RESULTS: Average alpha-1 band power density values in frontal and central regions were lower during the nicotine versus placebo condition, which provides evidence of nicotine-induced cortical activation. Furthermore, those with lower self-reported cognitive control exhibited greater nicotine-induced reductions in alpha-1 power density values.
CONCLUSIONS: These individual differences in nicotine-induced cortical activation are consistent with a model of nicotine self-medication whereby individuals with lower cognitive control may find smoking more reinforcing via amelioration of related cognitive deficits.
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