RATIONALE: Heavy smokers exhibit greater levels of impulsive choice and behavioural disinhibition than non-smokers. To date, however, the relationship between nicotine use and differing dimensions of impulsivity has not been systematically assessed. OBJECTIVES: A series of studies was designed to assess the acute dose-response effects of nicotine and the nicotinic receptor antagonist mecamylamine alone, and in combination with nicotine, on impulsive choice and behavioural disinhibition in rats. METHODS: Separate groups of rats were trained on a symmetrically reinforced go/no-go task to measure levels of disinhibition and a systematic delayed reward task to measure levels of impulsive choice. Once trained, all animals in each task were treated acutely with nicotine (0.125, 0.25, 0.5 and 1.0 mg/kg), mecamylamine (0.1, 0.3 and 1.0 mg/kg) and varying doses of mecamylamine (0.1, 0.3 and 1.0 mg/kg) prior to nicotine (0.5 mg/kg). An additional experiment assessed the effects of alterations in primary motivation (presatiation and fasting) on performance in both tasks. RESULTS: Acute nicotine increased both impulsive choice and behavioural disinhibition, effects that were blocked by pre-treatment with mecamylamine. Mecamylamine when administered alone did not alter impulsive behaviour. The lack of effect of presatiation on performance measures suggests that the observed nicotine-induced impulsivity cannot be attributed to the anorectic activity of the compound. CONCLUSIONS: Present findings support the hypothesis that heightened impulsivity in smokers may in part be a consequence of the direct acute effects of nicotine. As such, drug-induced changes in impulsivity may play a critical role in the transition to and maintenance of nicotine dependence.
RATIONALE: Heavy smokers exhibit greater levels of impulsive choice and behavioural disinhibition than non-smokers. To date, however, the relationship between nicotine use and differing dimensions of impulsivity has not been systematically assessed. OBJECTIVES: A series of studies was designed to assess the acute dose-response effects of nicotine and the nicotinic receptor antagonist mecamylamine alone, and in combination with nicotine, on impulsive choice and behavioural disinhibition in rats. METHODS: Separate groups of rats were trained on a symmetrically reinforced go/no-go task to measure levels of disinhibition and a systematic delayed reward task to measure levels of impulsive choice. Once trained, all animals in each task were treated acutely with nicotine (0.125, 0.25, 0.5 and 1.0 mg/kg), mecamylamine (0.1, 0.3 and 1.0 mg/kg) and varying doses of mecamylamine (0.1, 0.3 and 1.0 mg/kg) prior to nicotine (0.5 mg/kg). An additional experiment assessed the effects of alterations in primary motivation (presatiation and fasting) on performance in both tasks. RESULTS: Acute nicotine increased both impulsive choice and behavioural disinhibition, effects that were blocked by pre-treatment with mecamylamine. Mecamylamine when administered alone did not alter impulsive behaviour. The lack of effect of presatiation on performance measures suggests that the observed nicotine-induced impulsivity cannot be attributed to the anorectic activity of the compound. CONCLUSIONS: Present findings support the hypothesis that heightened impulsivity in smokers may in part be a consequence of the direct acute effects of nicotine. As such, drug-induced changes in impulsivity may play a critical role in the transition to and maintenance of nicotine dependence.
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