The reinforcing effects of nicotine have been investigated by intravenous self-administration methods using mice, rats, dogs, squirrel monkeys, rhesus monkeys, baboons, and humans. Based on accumulated data related to these effects, it is clear that subjects show moderate self-administration of nicotine with no marked manifestation in contrast to excessive self-administration of cocaine with hyperactivity and of morphine with withdrawal syndrome. The magnitude of reinforcing effects of nicotine was judged to be lower than that of cocaine and other abused drugs by the progressive ratio schedule method although persistent self-administration behavior for nicotine was maintained under the second-order schedule with conditioned stimulus in monkeys. The brain mechanism producing the reinforcing effects of nicotine is considered to involve nicotinic receptors at the nucleus accumbens, prefrontal cortex or other regions, as well as the mesolimbic dopaminergic system. It has been demonstrated by brain imaging techniques such as PET and fMRI that the relevant brain sites for producing craving for abused drugs such as cocaine include the amygdala, dorsolateral frontal cortex and anterior cingulated cortex. Further studies should elucidate the mechanism of craving for cigarettes by these imaging techniques. The actions of nicotine and its analogs have been studied for the purpose of developing therapeutic drugs for Alzheimer's disease, Parkinson's disease, Tourrette's syndrome and so on. Thus, studies on nicotine and its analogs with a wide variety of pharmacological profiles are interesting and important in the field of neuropsychopharmacology.