This finding is in accordance

with studies reporting hypoactivation in dorsal ACC during failed inhibition in cocaine and opiate addiction Selisistat datasheet ( Forman et al., 2004 and Kaufman et al., 2003). Moreover, in other task paradigms, similar findings have been reported. In two positron emission tomography studies, reduced activation in dorsal ACC during performance of a Stroop task was found in cocaine and marijuana abusers, relative to healthy controls ( Bolla et al., 2004 and Eldreth et al., 2004). This indicates that not only during error commission, but also during high-conflict trials dorsal ACC is hyporeponsive in substance-abusing populations, supporting the hypothesis that dorsal ACC has a general role in conflict monitoring, not only in error detection. Measuring event-related potentials, Franken et al. (2007), who used an Eriksen flanker task, found that the error-related negativity that originates from dmPFC was smaller for cocaine dependent subjects than healthy controls. The present study, therefore, extends the findings of hyporesponsiveness of dorsal ACC during error monitoring in substance abusers to PRG and HSM. We failed

to demonstrate performance differences between the groups: SSRTs did not differ between PRG, HSM and healthy controls. Several explanations may Sorafenib order be put forward for this negative finding. Firstly, impairments in response inhibition reported in other studies in patients with substance dependence might have been largely due to neurotoxicity of the involved substance. This is probably less of an issue in the present study. In the case of HSM, evidence is mixed, with one study reporting impaired response inhibition in HSM (Spinella, 2002) whereas other studies did not find such impairment (Dinn et al., 2004, Reynolds et al., 2007 and Monterosso et al., 2005). This discrepancy is likely to be due to differences in task paradigm and study population. In the case of PG, Goudriaan et al. (2006) did report increases in SSRT in pathological gamblers compared to healthy controls. SSRTs were overall much shorter in their study than

in the present almost study (for healthy controls: 114 ms vs. 270 ms in the present study), which raises the possibility that differences in task design, like the auditory stop signal in the study by Goudriaan and coworkers, vs. our visual stop signal, may have influenced results. Auditory stop signals render shorter SSRTs due to faster sensory processing of auditory cues compared to visual cues. Thus, our lack of behavioral differences between groups may be due to slower processing of the visual stop cues in our fMRI stop task, which could have limited sensitivity to detect group differences on a behavioral level. However, our combined findings on performance and BOLD activation could also be interpreted completely differently.