Abstract
Several experimental approaches have been used to delineate the initial sites and the distributions of action of nicotine in the brain. Radioligand binding studies have revealed a heterogeneous distribution of high affinity, specific binding sites for nicotine in brain. Other studies have employed metabolic mapping with 2-deoxy-D-[l-14C]glucose (DG) to measure of the regional cerebral metabolic rate(s) for glucose (rCMRglc). In rats, l-nicotine stimulates rCMRglc in brain areas which contain specific binding sites for [3H]nicotine, indicating that the sites are true receptors, linked to functional activity. Affected areas include limbic structures, components of the visual system, brain stem nuclei important in cardiovascular reflexes, and areas involved in motor function. In general, rats show tolerance to the effects of nicotine on rCMRglc. The distribution of in vivo effects of nicotine on rCMRglc implicates various brain regions in the behavioral and physiological effects of the drug.
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