Alpha coupling effects.

<p>(A) Alpha coupling between 900–1100 ms is shown. Displayed connections show significantly increased coupling from ipsilateral motor cortex to corresponding electrodes for EG- compared to EC-trials and for EN- compared to EC-trials. (B) Exemplary time-courses of the PLV. On the left, synchrony between contralateral motor cortex and a same-side prefrontal electrode (F5/F6) and on the right synchrony between ipsilateral motor cortex and a same-side prefrontal electrode (F5/F6) is displayed. Note that there was a significant difference for connectivity to ipsilateral but not to contralateral M1.</p

Ready for change: Oscillatory mechanisms of proactive motor control

<div><p>Proactive motor control is a preparatory mechanism facilitating upcoming action inhibition or adaptation. Previous studies investigating proactive motor control mostly focused on response inhibition, as in the classical go-nogo or stop-signal tasks. However, everyday life rarely calls for the complete suppression of actions without subsequent behavioral adjustment. Therefore, we conducted a modified cued go-nogo-change task, in which cues indicated whether participants might have to change to an alternative action or inhibit the response to an upcoming target. Based on the dual-mechanisms of control framework and using electroencephalography (EEG), we investigated the role of the sensorimotor cortex and of prefrontal regions in preparing to change and cancel motor responses. We focused on mu and beta power over sensorimotor cortex ipsi- and contralateral to an automatic motor response and on prefrontal beta power. Over ipsilateral sensorimotor cortex, mu and beta power was relatively decreased when anticipating to change or inhibit the automatic motor behavior. Moreover, alpha phase coupling between ipsilateral motor cortex and prefrontal areas decreased when preparing to change, suggesting a decoupling of sensorimotor regions from prefrontal control. When the standard motor action actually had to be changed, prefrontal beta power increased, reflecting enhanced cognitive control. Our data highlight the role of the ipsilateral motor cortex in preparing to inhibit and change upcoming motor actions. Here, especially mu power and phase coupling seem to be critical to guide upcoming behavior.</p></div

Sensorimotor effects in the cue-target interval.

<p>(A) On the left timecourses of mu (9-14 Hz) and beta (15–25 Hz) power at contralateral and ipsilateral sensorimotor clusters in relation to the standard motor response are displayed. The modulation of mu power was strongest over the ipsilateral hemisphere. Between 500–1100 ms mu increased in expecting go (EG), was around baseline in expecting nogo (EN) and decreased clearly in expecting change (EC). As shaded area around the mean, the SEM is displayed. Target onset was at 1100 ms (dotted line). Horizontal bars under the time axis highlight time-windows with significant differences between conditions. Black bars highlight windows where EG & EC significantly differed, dark grey bars where EG & EN differed and light grey bars where EN & EC differed. To the right bar graphs show mean mu/beta power between 500–1100 ms at contralateral and ipsilateral sensorimotor sites. As error bars the SEM is depicted. Significant differences are stressed with asterisks. (B) Time-frequency plots of activity in the EG condition at contra- and ipsilateral sensorimotor clusters. (C) The topographic plots show the scalp distribution of the mean signal change (500–1100 ms) as differences between EC and EG. All data in this figure is flipped along the midline.</p

Target-evoked prefrontal beta power (15–25 Hz).

<p>(A) Timecourse of beta power at left and right prefrontal clusters. As shaded area the SEM is displayed and the time-window we analyzed (200–500 ms) is marked with a grey box. Significant differences are indicated with asterisks. (B) At both left and right prefrontal clusters beta power was higher in change- and nogo- than no-change-/no-nogo-trials and lowest in go-trials. As error bars the SEM is depicted. (C) Topographic plots show the scalp distribution of the mean signal change (200–500 ms) in the beta band as difference between conditions.</p

Experimental setup.

<p>The photos show the typical facial expressions induced by the chop stick in the smile and no-smile conditions.</p

Post-error slowing.

<p>Correct responses following erroneous responses (posterror trials) are compared with correct responses following response-matched correct responses (postcorrect trials). Reaction times are given in milliseconds.</p

Design and behavioral results.

<p>(A) Design of the cued go-nogo-change task. In expecting go-trials, the cue (black square) was always followed by a black triangle, indicating a right button press. In expecting change-trials, the cue (green square) was followed in 75% by a black triangle, indicating a right button press and in 25% by a green triangle, indicating a left button press. In expecting nogo-trials, the cue (red square) was followed in 75% by a black triangle, indicating a right button press and in 25% by a red triangle, indicating no button press. In the second half of the experiment, the matching of the response buttons was reversed (meaning expecting go-trials required a left button press etc.). (B) Reaction times. Mean reaction times in ms in go-, no-change-, no-nogo- and change-trials. As error bars the standard error of the mean (SEM) is depicted. Participants responded faster in go- than no-change-/no-nogo- than change-trials. Significant effects are indicated with asterisks (* for ≤ 0.05, ** for ≤ 0.01, *** for ≤ 0.001).</p

Overview of utilized contrasts in the study.

<p>Overview of utilized contrasts in the study.</p

Trial timing and behavioural results.

<p><b>A</b> Time course of a single trial under high provocation. The trial began with a 12-s preparation phase. The participant saw the opponent for the upcoming trial and had to select the punishment. After the reaction-time task proper, the participant was informed about the selection of the opponent. Finally feedback was given about the outcome and the participant had to either press a button for the punishment or the temperature of the thermode was increased. <b>B</b> Average punishment selections under low (grey) and high (black) provocation separately for low (filled bars) and high (stripes) trait aggressive participants (median split; n = 28). <b>C</b> Average punishment selection in low (grey) and high (black) provocation trials, separately for the tryptophan depleted (TRP-) and balanced (BAL) group across the four runs.</p

Imaging results for the outcome phase (first run).

<p><b>A</b> depicts the results of the correlational analysis for the outcome phase during the first run. Participants with a higher behavioral provocation effect showed an increased neural provocation effect in the caudate nucleus, dorsal ACC, insula and right inferior frontal gyrus. <b>B</b> For visualization purpose only, the correlation of the average difference in beta values in the caudate nucleus (left) and ACC (right) with the behavioral provocation effect (effect size d, selection high – low provocation, relative to the pooled standard deviance) is shown with the best linear fit. Participants of the TRP- group are indicated with a cross; BAL participants are shown with a circle.</p