The incentive sensitization theory of addiction posits that addiction arises from drug-induced sensitization in the brain's mesocorticolimbic systems, which assign incentive salience to reward-associated stimuli. This sensitization leads to pathological incentive motivation ('wanting') for drugs. The theory emphasizes the role of learning in sensitization, the development of addiction-like behaviors in animals, and the relevance of affective pleasure or withdrawal in addiction. It also addresses whether incentive sensitization occurs in human addicts and how to model addiction symptoms using animal models. The theory suggests that repeated exposure to drugs can sensitize brain circuits that regulate the attribution of incentive salience to stimuli, leading to compulsive drug-seeking behavior. Learning specifies the object of desire but is not sufficient for pathological motivation. Instead, it is the sensitization of brain circuits mediating Pavlovian conditioned incentive motivational processes that drives pathological motivation. Associative learning can modulate the expression of neural sensitization in specific contexts. Incentive sensitization is distinct from learning and involves hypersensitivity in brain circuits that mediate incentive motivation. Evidence for incentive sensitization includes increased behavioral and neural responses to drug-associated stimuli, such as enhanced conditioned approach behavior, Pavlovian instrumental transfer, and conditioned reinforcement. These effects are consistent with the theory and have been observed in both animals and humans. In humans, repeated amphetamine administration can produce persistent behavioral sensitization, and drug cues can elicit vigorous dopamine responses in reward-related brain structures. However, there are conflicting results regarding brain dopamine changes in addicts, and the context in which drug use occurs is crucial for the expression of sensitization. Animal studies show that extended access to drugs facilitates the development of addiction-like symptoms and cognitive deficits. Extended access to cocaine produces symptoms of prefrontal cortex dysfunction and cognitive deficits, similar to those seen in human addicts. Extended access also produces robust psychomotor sensitization, suggesting that it is an effective model for studying the transition from casual to compulsive drug use. The theory also addresses the role of affective processes in addiction, distinguishing between wanting and liking. Drugs initially produce pleasure, but with addiction, the role of pleasure decreases while the desire for drugs increases. This dissociation between wanting and liking is central to the theory and explains why addicts continue to seek drugs despite negative consequences. In conclusion, addiction involves drug-induced changes in brain circuits that lead to complex behavioral and psychological changes. The core changes leading to addiction occur when incentive sensitization combines with defects in cognitive decision making. The theory suggests that addiction is a disorder of aberrant incentive motivation due to drug-induced sensitization of neural systems that attribute salience to particular stimuli. It can be triggered by drug cues as a learned motivational response but is not a disorder of aberrant learning per se. Sensitized wanting may compel drug pursuit regardless of withdrawal symptoms, and incentive salience is distinct from pleasure or liking processes, giving impulsive drug wanting an enduring life of its own.The incentive sensitization theory of addiction posits that addiction arises from drug-induced sensitization in the brain's mesocorticolimbic systems, which assign incentive salience to reward-associated stimuli. This sensitization leads to pathological incentive motivation ('wanting') for drugs. The theory emphasizes the role of learning in sensitization, the development of addiction-like behaviors in animals, and the relevance of affective pleasure or withdrawal in addiction. It also addresses whether incentive sensitization occurs in human addicts and how to model addiction symptoms using animal models. The theory suggests that repeated exposure to drugs can sensitize brain circuits that regulate the attribution of incentive salience to stimuli, leading to compulsive drug-seeking behavior. Learning specifies the object of desire but is not sufficient for pathological motivation. Instead, it is the sensitization of brain circuits mediating Pavlovian conditioned incentive motivational processes that drives pathological motivation. Associative learning can modulate the expression of neural sensitization in specific contexts. Incentive sensitization is distinct from learning and involves hypersensitivity in brain circuits that mediate incentive motivation. Evidence for incentive sensitization includes increased behavioral and neural responses to drug-associated stimuli, such as enhanced conditioned approach behavior, Pavlovian instrumental transfer, and conditioned reinforcement. These effects are consistent with the theory and have been observed in both animals and humans. In humans, repeated amphetamine administration can produce persistent behavioral sensitization, and drug cues can elicit vigorous dopamine responses in reward-related brain structures. However, there are conflicting results regarding brain dopamine changes in addicts, and the context in which drug use occurs is crucial for the expression of sensitization. Animal studies show that extended access to drugs facilitates the development of addiction-like symptoms and cognitive deficits. Extended access to cocaine produces symptoms of prefrontal cortex dysfunction and cognitive deficits, similar to those seen in human addicts. Extended access also produces robust psychomotor sensitization, suggesting that it is an effective model for studying the transition from casual to compulsive drug use. The theory also addresses the role of affective processes in addiction, distinguishing between wanting and liking. Drugs initially produce pleasure, but with addiction, the role of pleasure decreases while the desire for drugs increases. This dissociation between wanting and liking is central to the theory and explains why addicts continue to seek drugs despite negative consequences. In conclusion, addiction involves drug-induced changes in brain circuits that lead to complex behavioral and psychological changes. The core changes leading to addiction occur when incentive sensitization combines with defects in cognitive decision making. The theory suggests that addiction is a disorder of aberrant incentive motivation due to drug-induced sensitization of neural systems that attribute salience to particular stimuli. It can be triggered by drug cues as a learned motivational response but is not a disorder of aberrant learning per se. Sensitized wanting may compel drug pursuit regardless of withdrawal symptoms, and incentive salience is distinct from pleasure or liking processes, giving impulsive drug wanting an enduring life of its own.