Paradoxical, causal effects of sensory gain modulation on motor inhibitory control - a tDCS, EEG-source localization study.

Response inhibition is a key component of executive functioning, but the role of perceptual processes has only recently been focused. Although the interrelation of incoming information and resulting behavioural (motor) effects is well-known to depend on gain control mechanisms, the causal role of sensory gain modulation for response inhibition is elusive. We investigate it using a somatosensory response inhibition (Go/Nogo) task and examine the effects of parietal (somatosensory) cathodal and sham tDCS stimulation on a behavioural and neurophysiological level. For the latter, we combine event-related potential (ERP) and source localization analyses. Behavioural results reveal that cathodal stimulation leads to superior inhibition performance as compared to sham stimulation depending on the intensity of tDCS stimulation. The neurophysiological data show that an early (perceptual) subprocess of the Nogo-N2 ERP-component is differentially modulated by the type of stimulation but not a later (response-related) Nogo-N2 subcomponent. Under cathodal stimulation, the early N2 amplitude is reduced and the right inferior frontal gyrus (BA45) is less active. Cathodal tDCS likely enhances inhibition performance via decreasing the efficiency of gain control and the impact of sensory stimuli to trigger prepotent responses. Thereby, response inhibition processes, associated with structures of the response inhibition network, become less demanded.