Sequential modulation of (bottom-up) response activation and inhibition in a response conflict task: a single-pulse...

Many cognitive tasks involve a response conflict between the response selected on the basis of the task-relevant attribute and that primed by an irrelevant attribute. Although response priming has been extensively investigated, we still have little evidence on whether it entails both excitatory and inhibitory processes and the way in which these processes are modulated by the prior occurrence of a conflict between-response alternatives. To shed light on these issues, we tested motor cortex excitability during a two-choice compatibility task (a Simon task) by delivering single pulses of transcranial magnetic stimulation and recording the resulting motor evoked potentials (MEPs). We obtained consistent behavioural and MEP results suggesting that the presentation of a left- or right-side stimulus causes the activation of the ipsilateral response, which-in turn-inhibits the alternative response. Both processes are modulated by the spatial compatibility of the preceding trial. In trials following compatible trials (i.e. after conditions wherein the primed response was the correct one), we found response efficiency advantages and disadvantages of compatible and incompatible trials, respectively, which were mirrored by an increase of the excitability of the motor cortex primed by stimulus position and by a parallel decrease of the contralateral cortex excitability. Both the facilitation and interference components of the behavioural effect and the excitatory and inhibitory effects of the stimulus position on motor excitability were smaller after neutral trials (i.e. when the stimulus of the previous trial was aligned with fixation, thus not priming any response) and absent after incompatible trials (i.e. after having experienced a conflict between the primed and correct responses). These results are consistent with the idea that location-based response priming is under control of a conflict monitoring mechanism that strengthens ipsilateral response activation and contralateral response inhibition after compatible trials and weakens both processes after incompatible trials.