Impulsivity can be defined as the tendency to act prematurely without foresight. Behavioural and neurobiological analysis of this construct, based on evidence from both animal and human studies, defines several dissociable forms depending on distinct cortico-striatal substrates. One form of impulsivity depends on the temporal discounting of reward, and another on motor or response disinhibition. Impulsivity is commonly associated with addiction to drugs from different pharmacological classes, but its causal role in human addiction is unclear. I will characterize in neurobehavioral and neurochemical terms a rodent model of impulsivity based on premature responding in an attentional setting. Evidence will be surveyed that high impulsivity on this task precedes the escalation subsequently of cocaine self-administration behavior, as well as a tendency toward compulsive cocaine-seeking and to relapse. These results indicate that the vulnerability to stimulant addiction may depend on an impulsivity endophenotype. Implications of these findings for the aetiology, development, and treatment of drug addiction are considered in the light of recent evidence from studies of human chronic stimulant abusers and their non-drug abusing siblings. I will also consider the neuropsychological basis of compulsivity which can be defined as aberrant perseverative behaviour, and for which obsessive-compulsive behaviour (OCD) is probably the prototypical disorder. I will identify (i) distinct cortical-striatal substrates for compulsive responding which reflect the neural bases of goal-directed and habit learning and (ii) candidate neuroendophenotypes for OCD. I will also address the issue of possible commonalities and differences in the compulsivity of chronic substance abuse and OCD.