Exploring the mechanisms underlying the phenomenon of inner speaking-induced suppression

Speaking-induced suppression (SIS) refers to the phenomenon that the sounds produced through self-generated speech elicit less EEG activity in the auditory cortex than externally-produced sounds. An analogous phenomenon demonstrates that the activity elicited by an audible syllable is suppressed when it co-occurs with a content-matching syllable produced in inner speech. We have argued that this ‘inner SIS’ effect is likely underpinned by corollary discharges, similar to those assumed to underlie SIS. However, an alternative possibility is that ‘inner SIS’ reflects a priming effect, wherein the increased subjective expectation of hearing a certain sound causes a reduction in evoked activity. The current study tested this alternative hypothesis using an expectancy-only version of the task in which participants (N=70, 45 female and 25 male) did not produce inner speech. On each trial, a syllable appeared on-screen (/ba/, /bi/, or /fo/), and was followed by an audible syllable (/ba/ or /bi/). The on-screen syllable either matched (Primed condition) or mismatched (Misprimed condition) the content of the audible syllable. In the Control condition, the on-screen syllable never occurred as the audible syllable. Contrary to previous studies in which participants produced inner speech, there were no significant between-condition differences in N1-amplitude, P2-amplitude, pre-stimulus activity or gamma-band power elicited by the audible syllable. Bayesian analysis indicated a meaningful difference between these findings and prior results from the inner speech task. The present data indicate that a simple cue-based priming manipulation, in the absence of inner speech, is insufficient to reproduce previously reported inner-SIS effects. Significance statement Inner speaking-induced suppression (‘inner SIS’) refers to the phenomenon that the electrophysiological activity elicited by an external vocalization is reduced when participants concurrently produce the same vocalization in their inner speech. We, and others, have argued that inner SIS is likely caused by corollary-discharge-related mechanisms. However, an alternative possibility is that inner SIS reflects a priming effect, wherein the increased subjective expectation of hearing a certain vocalization causes a reduction in evoked activity. Using a modified version of our standard experimental protocol, we found no evidence for this alternative hypothesis. This result suggests that a priming manipulation, in the absence of inner speech, is insufficient to reproduce previously reported inner-SIS effects.