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Nicotine Tob Res. 1999;1 Suppl 2:S127-32; discussion S139-40.

Imaging the neurochemistry of nicotine actions: studies with positron emission tomography.

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  • 1Medical Department, Brookhaven National Laboratory, Upton, NY 11973, USA.


Although the effects of nicotine in the brains of laboratory animals have been investigated extensively, very little is known about its effects in the human brain. With positron emission tomography (PET), a non-invasive imaging technology that allows measurement of the concentration of positron-labeled compounds that are of physiological and pharmacological relevance, it has become possible to investigate the effects of nicotine in the human brain. These imaging studies have shown that nicotine has very fast pharmacokinetics in the human brain, that it changes cerebral blood flow (CBF) and brain metabolism, and that at least some of these effects show acute tolerance. PET studies have also shown that, in addition to nicotine, cigarettes possess other pharmacological actions that may contribute to their reinforcing effects, that cigarettes inhibit monoamine oxidase (MAO) A and B in the brain, and that this inhibition recovers with cigarette discontinuation. Although the nicotine receptors have not yet been imaged in the living human brain, PET studies in the primate brain have shown very high concentration of receptors in the thalamus and a high rate of blockade by doses of nicotine that approximate plasma levels achieved by humans when smoking cigarettes. However, further studies are required to determine the levels of nicotine receptor occupancies achieved when smoking a cigarette and those required for the nicotine patch to be therapeutically effective, to measure the half-life for MAO inhibition by cigarettes and the mechanisms underlying this inhibition, and to evaluate the effects of smoking on nicotine receptors and on other neurotransmitter systems in the human brain.

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