Brain regions associated with arousal, compulsive repetitive behaviors, sensory integration, and episodic memory are activated during exposure to cigarette-related cues and cigarette craving. These regional brain activations and associations with craving are similar to findings with other addictive substances.

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This study was designed to demonstrate that dopaminergic stimulation would result in decreased smoking behavior and nicotine intake, whereas dopaminergic blockade would result in increased smoking behavior and nicotine intake, in the same subjects. In prior human studies, a dopaminergic antagonist, haloperidol, increased smoking and/or nicotine intake, and a dopamine agonist, bromocriptine, decreased smoking. The smoking behavior of 20 heavy smokers was observed on two separate visits in a randomized, double-blind, repeated-measures-within-subject design. In the drug-reversal design, either bromocriptine (2.5 mg) or haloperidol (2.0 mg) was administered at each 5-h session, during which subjects smoked their own cigarettes ad libitum. Smoking topography was measured using a thermistor flow detector apparatus. Subjects smoked their cigarettes faster (p<0.05) and total puffing time was greater (p<0.05) with haloperidol than with bromocriptine. There was a trend for both a shorter latency to smoke (p<0.10, one-tailed) during time of expected peak drug concentration and for a shorter inter-cigarette interval with haloperidol than with bromocriptine (p<0.10, one-tailed). Shiffman-Jarvik Withdrawal Scale craving subscale scores increased significantly more with haloperidol than with bromocriptine (p<0.05). Mean Profile of Mood States (POMS) scores differed significantly for only one subscale (Confusion: bromocriptine>haloperidol; p<0.05). These data support the hypothesis that nicotine mediates reinforcement from smoking via dopamine, and that smoking behavior can be manipulated within the same subjects in opposite directions by alternately stimulating and blocking dopamine.