example, intravenous cocaine (which increases extracellular dopamine levels) in cocaine users improved inhibitory control in a go/no-go task, and this was associated with normalization of ACC activity and enhanced right DLPFC activation during the task134. Intravenous MPH (which also increases extracellular dopamine levels) similarly improved performance on the SSRT in cocaine abusers, and this was positively correlated with inhibition-related activation of the left middle frontal cortex and negatively correlated with activity in the ventromedial PFC; after MPH, activity in both regions showed a trend for normalization135. A PET study showed that oral MPH attenuated the reduced metabolism in limbic brain regions — including lateral OFC and DLPFC — that followed exposure to cocaine-related cues in cocaine-addicted individuals136. It also decreased errors of commission, a common measure of impulsivity, during a drug-relevant emotional Stroop task, both in cocaine-addicted individuals and controls, and in the addicted individuals this decrease was associated with normalization of activation in the rostroventral ACC (extending to the mOFC) and dACC; dACC task-related activation before MPH administration was correlated with shorter lifetime alcohol use137 (FIG. 4). Although it remains to be studied whether or how the noradrenergic effects of MPH contribute to its ‘normalizing’ effects in cocaine users,
