In addition, subcortical activations in bilateral striatum and thalamus were found. The Failed stop > control contrast was associated www.selleckchem.com/Proteasome.html with activation in dorsal ACC (BA24) and pre-SMA (BA6). Also, right inferior frontal gyrus/insula region and right dorsolateral prefrontal cortex were activated. In addition, we found activation of bilateral posterior parietal cortex and left precuneus ( Table 2, also for Brodmann areas). For the Successful inhibition > control contrast, ROI analysis revealed significantly lower activation in both PRG and HSM compared to healthy controls in a region of dmPFC bordering on BA8 and

dorsal ACC (BA32) ( Table 3a; Fig. 1, Fig. 2 and Fig. 3). For the Failed

inhibition > control contrast, ROI analysis showed that, relative to healthy controls, both PRG and HSM showed hypoactivation in dorsal ACC (BA32). For HSM, we found additional hyperactivity in frontopolar cortex compared to healthy controls. Including BDI and CAARS scores only had a marginal effect on the results. ( Table 3b; Fig. 1, Fig. 2 and Fig. 3). For the Successful inhibition > control contrast, we found a significant negative correlation of SOGS scores and BOLD activation in the right dmPFC (anterior cingulate, BA32) in PRG (MNI coordinates [15,39,40], Z score = 4.17, P < 0.001, PSVC < 0.01, r = 0.85). BMN 673 mouse No other significant correlations were found. Conjunction analyses were carried out to formally assess the brain regions that showed conjoint hypoactivations for PRG and HSM compared to healthy controls. For the Successful inhibition > control contrast, we found hypoactivation in dmPFC ( Table 3a). For the Failed inhibition > control contrast, we found dorsal ACC (BA32). The latter effect was only found when lowering our threshold for inspection (uncorrected

significance: P = 0.0016, Table 3b). Whole-brain group analyses showed no significant effects. The present study aimed to investigate the neural circuitry associated with inhibitory control in PRG and HSM. We therefore focused on both no successful and failed response inhibition in a stop signal task, using a paradigm which included control conditions tailored to specifically isolate neural correlates of response inhibition and conflict/error monitoring. The first hypothesis was not confirmed: PRG and HSM showed similar accuracy and similar SSRT compared to non-smoking and non-gambling healthy controls. However, the second hypothesis was confirmed: both PRG and HSM showed hypoactivation of dmPFC during inhibitory control when compared to non-smoking and non-gambling healthy controls.