Impairments in inhibitory control, an essential neuropsychological function for stopping unwanted behaviors, are core to drug addiction pathology [1]. The neural substrates of inhibitory control are rooted in the cognitive control network including the dorsolateral prefrontal cortex (dlPFC), supplementary motor area (SMA), and inferior frontal gyrus [2]. Recently, we have published common and unique findings across individuals with cocaine and heroin use disorders (iCUD, iHUD), providing neurobiological evidence for inhibitory control deficits and their potential recovery with treatment.

First, we modified the stop-signal task (a classic inhibitory control measure) to include cocaine-related and competing nondrug salient words (e.g., food) in an enriched fMRI task to inspect inhibitory control under drug and nondrug contexts in 26 iCUD and 26 matched healthy controls. Word stimuli served as go signals requiring a button press and stop-signals when their color turned red. Regardless of cue type, we found lower anterior PFC (aPFC), and during cocaine vs. food word inhibition, lower dlPFC activity; higher activity here correlated with recent use frequency, craving, and shorter abstinence [3]. These results suggest the potential need for dlPFC deactivation in the face of drug cues to perform similarly to controls.