http://www.ncbi.nlm.nih.gov/pubmed/9549600
This isn't a new observation, of course. What I wonder, however, is why I have heard of no adverse drug reactions when combining tobacco with recreational drugs (as is surely extremely common). Is this activity just too weak to be acutely significant?
PubMed said: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.
We measured the concentration of brain monoamine oxidase B (MAO B; EC 1.4.3.4) 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.
This isn't a new observation, of course. What I wonder, however, is why I have heard of no adverse drug reactions when combining tobacco with recreational drugs (as is surely extremely common). Is this activity just too weak to be acutely significant?
