, 2003) and the automated anatomical labelling (AAL) atlas ( Tzourio-Mazoyer et al., 2002) of SMA, angular gyrus, insula, superior frontal medial cortex and precuneus. The resulting statistical maps were overlaid onto a normalized T1-weighted MNI template (colin27) and the coordinates reported correspond to the MNI coordinate system. The repeated-measures ANOVA revealed a significant main effect for agency [F(1,17) = 5.96, p < .05] with participants giving significantly shorter interval estimates in the active compared to the passive condition on the judgement error. There was

an unsurprising significant main effect of delay [F(2,34) = 16.49, p < .001] with more pronounced underestimation of the action–effect interval at longer delays. There was also a significant interaction of both factors [F(2,34) = 6.48, Alectinib purchase p < .01] ( Fig. 1). This interaction arose because selleck chemical the difference in judgement error between active and passive conditions increased with action-tone delay. The interval estimation task was analysed by parametrically modulating the action onset

with the judgement error of the action-tone interval. We then contrasted the active with the passive condition based on the fact that the active condition should involve a shortening of the awareness of the interval, whereas the passive condition should not. This analysis identifies brain regions that correlate with the compression of the action-tone interval more strongly in the active than in the passive condition. The previous literature gave strong predictions about involvement of specific regions in the experience of agency: the angular gyrus and the SMA (see Etofibrate Introduction) but also insula, frontomedian cortex and precuneus. Therefore we used a small volume correction within anatomically defined mask of these structures of interest. We identified a significant cluster within the SMA ROI family-wise error corrected p < .05 after small volume correction at −11, −8, 74 (cluster

size = 7 voxels) ( Fig. 2). Closer inspection confirmed that the cluster was located in left BA6, effectively on the margin between the lateral portion of BA6 comprising the dorsal premotor cortex, and the medial portion comprising the SMA proper. We applied a similar small volume correction to the bilateral angular gyrus, insula, frontomedian cortex and precuneus ROI, but found no significant difference between the parametric regressors for the active and passive conditions (nor in the reverse contrast) surviving correction within these areas. A whole brain analysis of the contrast between the parametric regressors for the active and passive condition with a statistical criterion of p < .001 uncorrected for multiple comparisons again revealed the same SMA cluster at −11, −8, 74, but no other significant clusters. Further, no significant clusters of activation were found in the reverse contrast.