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Dominant neuroanatomical models hold that humans regulate their movements via loop-like cortico-subcortical networks, which include the subthalamic nucleus (STN), motor thalamus, and sensorimotor cortex (SMC). Inhibitory commands across these networks are purportedly sent via transient, burst-like signals in the β frequency (15–29 Hz). However, since human depth-recording studies are typically limited to one recording site, direct evidence for this proposition is hitherto lacking. Here, we present simultaneous multi-site recordings from SMC and either STN or motor thalamus in humans performing the stop-signal task. In line with their purported function as inhibitory signals, subcortical β-bursts were increased on successful stop-trials. STN bursts in particular were followed within 50 ms by increased β-bursting over SMC. Moreover, between-site comparisons (including in a patient with simultaneous recordings from SMC, thalamus, and STN) confirmed that β-bursts in STN temporally precede thalamic β-bursts. This highly unique set of recordings provides empirical evidence for the role of β-bursts in conveying inhibitory commands along long-proposed cortico-subcortical networks underlying movement regulation in humans. 

Abstract Classic work using the stop-signal task has shown that humans can use inhibitory control to cancel already initiated movements. Subsequent work revealed that inhibitory control can be proactively recruited in anticipation of a potential stop-signal, thereby increasing the likelihood of successful movement cancellation. However, the exact neurophysiological effects of proactive inhibitory control on the motor system are still unclear. On the basis of classic views of sensorimotor β-band activity, as well as recent findings demonstrating the burst-like nature of this signal, we recently proposed that proactive inhibitory control is implemented by influencing the rate of sensorimotor β-bursts during movement initiation. Here, we directly tested this hypothesis using scalp EEG recordings of β-band activity in 41 healthy human adults during a bimanual RT task. By comparing motor responses made in two different contexts—during blocks with or without stop-signals—we found that premovement β-burst rates over both contralateral and ipsilateral sensorimotor areas were increased in stop-signal blocks compared to pure-go blocks. Moreover, the degree of this burst rate difference indexed the behavioral implementation of proactive inhibition (i.e., the degree of anticipatory response slowing in the stop-signal blocks). Finally, exploratory analyses showed that these condition differences were explained by a significant increase in β bursting that was already present during baseline period before the movement initiation signal. Together, this suggests that the strategic deployment of proactive inhibitory motor control is implemented by upregulating the tonic inhibition of the motor system, signified by increased sensorimotor β-bursting both before and after signals to initiate a movement. 

The stop signal task (SST) is the gold standard experimental model of inhibitory control. However, neither SST condition–contrast (stop vs. go, successful vs. failed stop) purely operationalizes inhibition. Because stop trials include a second, infrequent signal, the stop versus go contrast confounds inhibition with attentional and stimulus processing demands. While this confound is controlled for in the successful versus failed stop contrast, the go process is systematically faster on failed stop trials, contaminating the contrast with a different noninhibitory confound. Here, we present an SST variant to address both confounds and evaluate putative neural indices of inhibition with these influences removed. In our variant, stop signals occurred on every trial, equating the noninhibitory demands of the stop versus go contrast. To entice participants to respond despite the impending stop signals, responses produced before stop signals were rewarded. This also reversed the go process bias that typically affects the successful versus failed stop contrast. We recorded scalp electroencephalography in this new version of the task (as well as a standard version of the SST with infrequent stop signal) and found that, even under these conditions, the properties of the frontocentral stop signal P3 ERP remained consistent with the race model. Specifically, in both tasks, the amplitude of the P3 was increased on stop versus go trials. Moreover, the onset of this P3 occurred earlier for successful compared with failed stop trials in both tasks, consistent with the proposal of the race model that an earlier start of the inhibition process will increase stopping success. Therefore, the frontocentral stop signal P3 represents a neural process whose properties are in line with the predictions of the race model of motor inhibition, even when the SST's confounds are controlled.