Neuropharmacological actions of cigarette smoke:
brain monoamine oxidase B (MAO B) inhibition

Fowler JS, Volkow ND, Wang GJ, Pappas N,
Logan J, MacGregor R, Alexoff D, Wolf AP,
Warner D, Cilento R, Zezulkova I
Department of Chemistry and Medicine,
Brookhaven National Laboratory, Upton, NY 11973, USA.
J Addict Dis 1998; 17(1):23-34


We measured the concentration of brain monoamine oxidase B (MAO B; EC in 8 smokers and compared it with that in 8 non-smokers and in 4 former smokers using positron emission tomography (PET) and deuterium substituted [11C]L-deprenyl ([11C]L-deprenyl-D2) as a radiotracer for MAO B. Smokers had significantly lower brain MAO B than non-smokers as measured by the model term lambda k3 which is a function of MAO B activity. Reductions were observed in all brain regions. Low brain MAO B in the cigarette smoker appears to be a pharmacological rather than a genetic effect since former smokers did not differ from non-smokers. Brain MAO B inhibition by cigarette smoke is of relevance in light of the inverse association between smoking and Parkinson's disease and a high prevalence of smoking in psychiatric disorders and in substance abuse. Though nicotine is at the core of the neuropharmacological actions of tobacco smoke, MAO B inhibition may also be an important variable in understanding and treating tobacco smoke addiction.
Free-base nicotine
Parkinson's disease
Smoking and MAO-A
Smoking and MAO-B
SSRIs and smokers' hearts
Nicotine, dopamine and reward
Alcohol, nicotine and the opioid system
Bupropion and nortriptyline help smokers quit

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