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Functional Brain Imaging of Tobacco Exposure in Humans

Steven S Storage and Arthur L Brody

Cigarette smoking represents a major health problem in the United States. Although most cigarette smokers express a desire to quit, only about 14 to 49% will be successful after 6 or more months of treatment. An improved understanding of the acute and chronic effects of smoking on brain function may lead to more efficacious pharmacological and behavioral treatments for smoking dependence. Many research groups have utilized functional brain imaging to examine the effects of tobacco exposure on brain activity. Acute administration of nicotine and cigarette smoking itself have been found to increase activity in the prefrontal cortex, thalamus, and visual system; reduce global brain activity; and increase dopamine (DA) release in the ventral striatum/nucleus accumbens. Chronic tobacco exposure lead to an overall up-regulation of α4β2 nicotinic acetylcholine receptors (nAChRs) across brain regions (other than thalamus), and reduced monoamine oxidase (MAO) A and B levels in the basal ganglia. Functional brain imaging studies of cigarette craving and withdrawal, too, demonstrate important changes in brain activity. Taken together, current research suggests that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits by either direct stimulation of nAChRs, indirect stimulation through DA release of MAO inhibition, or a combination of these, and perhaps, other factors. The purpose of this review is to provide a summary of current functional brain imaging studies of tobacco use and dependence, and use this information to develop a greater understanding of brain function in smokers.