Sensory Attenuation of Auditory P2 Responses is Modulated by the Sense of Action Timing Control

Sensory attenuation is a well-established phenomenon in which the neurophysiological response elicited by self-initiated stimuli is attenuated compared to identical externally generated stimuli. This phenomenon is mostly studied by comparing the N1 and P2 components of the auditory ERP. Sensory attenuation has also been linked to our sense of agency and control. In the present study, we investigated the role of action timing control in sensory attenuation. Previous studies that investigated the attenuation of the N1/P2 components instructed participants to generate self-initiated stimuli by having the participants perform a series of keypresses while EEG is recorded. ERP responses are then compared to a second condition where participants passively listen to identical sounds. Studies using this paradigm, known as the self-stimulation paradigm, have used a wide range of stimulus onset asynchronies (SOAs) for keypress timing. However, the choice of SOA is rarely explained, perhaps due to an assumption of trial independence. We found that as SOA increased, participants enacted more action timing control to maintain the specified SOA level. The degree of P2 suppression also increased as participants enacted more control. Contrary to most studies in the literature, we did not find N1 suppression but instead found N1 enhancement. The results suggest that P2 suppression may be related to action timing control while N1 enhancement may reflect factors other than motor predictions, in line with more recent interpretations of the N1 suppression effect.