Amplitude modulating frequency overrides carrier frequency in tACS-induced phosphene percept.

The amplitude modulated (AM) neural oscillation is an essential feature of neural dynamics to coordinate distant brain areas. The AM transcranial alternating current stimulation (tACS) has recently been adopted to examine various cognitive functions, but its neural mechanism remains unclear. The current study utilized the phosphene phenomenon to investigate whether, in an AM-tACS, the AM frequency could modulate or even override the carrier frequency in phosphene percept. We measured the phosphene threshold and the perceived flash rate/pattern from 12 human subjects (four females, aged from 20-44 years old) under tACS that paired carrier waves (10, 14, 18, 22 Hz) with different envelope conditions (0, 2, 4 Hz) over the mid-occipital and left facial areas. We also examined the phosphene source by adopting a high-density stimulation montage. Our results revealed that (1) phosphene threshold was higher for AM-tACS than sinusoidal tACS and demonstrated different carrier frequency functions in two stimulation montages. (2) AM-tACS slowed down the phosphene flashing and abolished the relation between the carrier frequency and flash percept in sinusoidal tACS. This effect was independent of the intensity change of the stimulation. (3) Left facial stimulation elicited phosphene in the upper-left visual field, while occipital stimulation elicited equally distributed phosphene. (4) The near-eye electrodermal activity (EDA) measured under the threshold-level occipital tACS was greater than the lowest power sufficient to elicit retinal phosphene. Our results show that AM frequency may override the carrier frequency and determine the perceived flashing frequency of AM-tACS-induced phosphene.

To Go or Not to Go: Degrees of Dynamic Inhibitory Control Revealed by the Function of Grip Force and Early Electrophysiological Indices.

A critical issue in executive control is how the nervous system exerts flexibility to inhibit a prepotent response and adapt to sudden changes in the environment. In this study, force measurement was used to capture "partial" unsuccessful trials that are highly relevant in extending the current understanding of motor inhibition processing. Moreover, a modified version of the stop-signal task was used to control and eliminate potential attentional capture effects from the motor inhibition index. The results illustrate that the non-canceled force and force rate increased as a function of stop-signal delay (SSD), offering new objective indices for gauging the dynamic inhibitory process. Motor response (time and force) was a function of delay in the presentation of novel/infrequent stimuli. A larger lateralized readiness potential (LRP) amplitude in go and novel stimuli indicated an influence of the novel stimuli on central motor processing. Moreover, an early N1 component reflects an index of motor inhibition in addition to the N2 component reported in previous studies. Source analysis revealed that the activation of N2 originated from inhibitory control associated areas: the right inferior frontal gyrus (rIFG), pre-motor cortex, and primary motor cortex. Regarding partial responses, LRP and error-related negativity (ERNs) were associated with error correction processes, whereas the N2 component may indicate the functional overlap between inhibition and error correction. In sum, the present study has developed reliable and objective indices of motor inhibition by introducing force, force-rate and electrophysiological measures, further elucidating our understandings of dynamic motor inhibition and error correction.