1. The separate and combined effects of monoamine oxidase A inhibition and nicotine on resting state EEG
- Author
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Vadim Ilivitsky, Dylan Smith, Derek J. Fisher, Verner Knott, and Pierre Blier
- Subjects
Male ,Nicotine ,Monoamine Oxidase Inhibitors ,Monoamine oxidase ,Moclobemide ,Pharmacology ,Electroencephalography ,Tobacco smoke ,03 medical and health sciences ,0302 clinical medicine ,Double-Blind Method ,medicine ,Humans ,Drug Interactions ,Pharmacology (medical) ,Nicotinic Agonists ,Cross-Over Studies ,medicine.diagnostic_test ,biology ,Drug Synergism ,Tobacco Use Cessation Devices ,030227 psychiatry ,Psychiatry and Mental health ,Nicotinic agonist ,Nicotine gum ,biology.protein ,Monoamine oxidase A ,Psychology ,030217 neurology & neurosurgery ,medicine.drug ,Clinical psychology - Abstract
While nicotine is often associated with the neuropsychological effects of tobacco smoke, the robust monoamine oxidase (MAO) inhibition observed in chronic smokers is also likely to play a role. Electroencephalographically-indexed alterations in baseline neural oscillations by nicotine have previously been reported in both smokers and non-smokers, however, little is known about the effects of MAO inhibition in combination with nicotine on resting state EEG. In a sample of 24 healthy non-smoking males, the effects of 6 mg nicotine gum, as well as MAO-A inhibition via 75 mg moclobemide, were investigated in separate and combined conditions over four separate test sessions. Drug effects were observed in the alpha2, beta2, and theta band frequencies. Nicotine increased alpha2 power, and moclobemide decreased beta2 power. Theta power was decreased most robustly by the combination of both drugs. Therefore, this study demonstrated that the nicotinic and MAO inhibiting properties of tobacco may differentially influence fast-wave oscillations (alpha2 and beta2), while acting in synergy to influence theta oscillations.
- Published
- 2015