Nicotine is the principle alkaloid in tobacco and is considered to be responsible for tobacco dependence due to its psychoactive properties and its capacity to induce self-administration behavior in animals. Its action affects the brain where it binds to specific nicotinic receptors distributed on the mesolimbic and mesocortial dopaminergic pathways. Dopamine release by the nerve endings on these pathways provokes activation of the cerebral response. Acute stimulation with nicotine provokes a rise in cerebral dopamine levels in the accumbens. Dopamine release is greatly lowered in animals having undergone chronic exposure to nicotine, suggesting desensitization of the nicotinic receptors. In the regular smoker, there is an increase in the number of cerebral nicotinic receptors which would be a neuroadaptation response to desensitization. Reduction in the serum nicotine level favors resensitization of the nicotinic receptors and their vacuity would be the cause of the withdrawal syndrome. In therapeutics, nicotinic substitutes can effectively suppress the withdrawal syndrome and lead to abstinence rates to the order of 20 to 25% at one year. Psychotropes can also be effective to help patients stop smoking. Their mechanism of action is not clearly established but most would act by increasing the level of cerebral dopamine. They are used independently of their antidepressor effect with abstinence rates to the order of 25 to 30% at one year. Their combination with nicotinic substitutes can increase the rate of success.