Likewise dopaminergics, nicotine can have specific vascular effects — most notably vasodilation. However, much of the observed vasodilatory effects appear to be mediated via NO . Intravenous administration of nicotine to human subjects leads to increased BOLD signal in the nucleus accumbens, amygdala, cingulate, and frontal lobes, all areas associated with reward circuitry . In addition, the primary sites of activation appear to correspond well with the distribution of nicotine cholinergic binding sites seen using nC-nicotine binding . The highest concentration of sites are seen in the frontal, cingulate, and insular lobes of the cortex and in the thalamus and basal ganglia. These results are somewhat different from those obtained using PET measurements of changes in regional CBF. Nicotine reduced rCBF in the left anterior temporal cortex and in the right amygdala. Increases were noted in the right anterior thalamus [164,165]. In the case of the MRI study nicotine was administered i.v. whereas in the PET studies it was administered nasally. How these two administration routes may affect the observed signal changes is not known.
Separation of the activation components due to the reward circuitry vs. those caused by direct stimulation of the cholinergic receptors has not been attempted, nor has a systematic investigation of the effects of other cholinergic antagonists or agonists upon the nicotine-induced hemodynamic changes. A further confound related to activation of reward circuitry vs. the direct effects of the drug on its target receptors has been pointed out by Hans Breiter and colleagues in their studies of monetary reward . In such studies one can obtain either positive or negative BOLD signal changes in the nucleus accumbens in response to the same stimulus depending upon what the expectation of the stimulus was. Thus, in cases where the drug is not administered in a double-blind fashion it is conceivable that the expectation of the subject may dramatically influence the activation seen in the accumbens! This is likely to be a confound in cases where the drug of interest, e.g., nicotine, does not produce a large change in dopamine release in the dopaminergic elements of the reward circuitry.
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