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

J. S. Fowler, N. D. Volkow, G. J. Wang, N. Pappas, J. Logan, R. Macgregor, D. Alexoff, A. P. Wolf, D. Warner, R. Cilento, I. Zezulkova

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109 Scopus citations


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 Xk 3 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 neurophar-macological actions of tobacco smoke, MAO B inhibition may also be an important variable in understanding and treating tobacco smoke addiction.

Original languageEnglish
Pages (from-to)23-34
Number of pages12
JournalJournal of Addictive Diseases
Issue number1
StatePublished - 24 Feb 1998
Externally publishedYes


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