Although the effects of patch type on selleck products craving trajectories were not significant, there was a notable tendency (p < .15) for nicotine patches to reduce craving relative to placebo patches over 44 days of smoking abstinence. No effects involving sex were found on postquit craving. Figure 1. TaqIA polymorphism affected craving for cigarettes across 44 days of smoking abstinence. Craving changes are normalized to prequit baseline. Dark lines show values that were predicted from the final hierarchical linear model. Gray lines show observed ... Discussion In this study, DRD2-related TaqIA polymorphism was related to reported motivation to smoke during both smoking and abstinence periods. A1 carriers were more likely than those with A2/A2 genotype to report smoking for psychomotor stimulation and to reduce negative affect.

In female smokers, the A1 individuals scored higher than A2/A2 carriers in expected probability and motive to smoke for cognitive enhancement. Female A1 subjects also reported a greater likelihood to smoke for pleasure than those of the A2/A2 genotype. Moreover, A1 carriers, regardless of sex, experienced more craving in early and later phases of a 6-week abstinence period, representing continued vulnerability to lapse and relapse. Effects on smoking for stimulation and cognitive enhancement One major finding from this study is that the A1 allele is linked to enhanced motives for smoking in situations associated with a desire for stimulation. In female but not in male subjects, A1 carriers were also more inclined to attribute their reasons for smoking to obtaining cognition-enhancing effects.

Nicotine has long been recognized as having psychostimulant-like action through activation of the mesolimbic DA pathway, a property closely related to its positive reinforcing effect (Wise & Bozarth, 1987). Nicotine increases locomotor activity in rats (Iwamoto, 1984). It also boosts psychomotor performance in humans, particularly when fatigue and boredom are factors in performance (Wesnes & Warburton, 1983). Besides nicotine’s well-known arousing effects in general (Gilbert, 1995), recent studies increasingly emphasize its effects in enhancing cognitive function in both animal models and humans (Levin, McClernon, & Rezvani, 2006).

Effects of addictive drugs, including nicotine, on cognitive functioning have been thought to be AV-951 mediated by the cortico-striatal-thalamic circuitry, and the DA neurotransmission is an important modulator of this network (Brody, 2006; Koob & Le Moal, 2001). The present data highlight a need for detailed investigations of how the TaqIA polymorphism regulates functions of and connectivity among specific brain sites in this network which lead to individual differences in cognitive enhancement�Crelated craving (Brody; Wang et al., 2007).