The article provides a comprehensive overview of the neurobiology of addiction, focusing on the three stages of the addiction cycle: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation (craving). Each stage involves distinct neurobiological mechanisms and changes in brain circuits, particularly the basal ganglia, extended amygdala, and prefrontal cortex. The binge/intoxication stage is characterized by increased incentive salience and habit formation, driven by changes in dopamine and opioid peptides in the basal ganglia. The withdrawal/negative affect stage involves decreased reward function and increased stress-like states, mediated by changes in the reward system and recruitment of stress neurotransmitters such as corticotropin-releasing factor (CRF) and dynorphin in the extended amygdala. The preoccupation/anticipation stage is marked by compromised executive function and increased craving, involving the dysregulation of circuits from the prefrontal cortex and insula to the basal ganglia and extended amygdala. The article also discusses molecular and genetic targets for treatment, the role of developmental exposure in vulnerability, and the relevance of these findings to non-drug addictions. Finally, it highlights the potential for novel pharmacotherapeutic, brain stimulation, and behavioral treatments based on a deeper understanding of the neurocircuitry of addiction.The article provides a comprehensive overview of the neurobiology of addiction, focusing on the three stages of the addiction cycle: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation (craving). Each stage involves distinct neurobiological mechanisms and changes in brain circuits, particularly the basal ganglia, extended amygdala, and prefrontal cortex. The binge/intoxication stage is characterized by increased incentive salience and habit formation, driven by changes in dopamine and opioid peptides in the basal ganglia. The withdrawal/negative affect stage involves decreased reward function and increased stress-like states, mediated by changes in the reward system and recruitment of stress neurotransmitters such as corticotropin-releasing factor (CRF) and dynorphin in the extended amygdala. The preoccupation/anticipation stage is marked by compromised executive function and increased craving, involving the dysregulation of circuits from the prefrontal cortex and insula to the basal ganglia and extended amygdala. The article also discusses molecular and genetic targets for treatment, the role of developmental exposure in vulnerability, and the relevance of these findings to non-drug addictions. Finally, it highlights the potential for novel pharmacotherapeutic, brain stimulation, and behavioral treatments based on a deeper understanding of the neurocircuitry of addiction.