Action-stopping is a canonical executive function thought to involve top-down control over the motor system. Here we aimed to validate this stopping system using high temporal resolution methods in humans. We show that, following the requirement to stop, there was an increase of right frontal beta (~13 to 30 Hz) at ~120 ms, likely a proxy of right inferior frontal gyrus; then, at 140 ms, there was a broad skeletomotor suppression, likely reflecting the impact of the subthalamic nucleus on basal ganglia output; then, at ~160 ms, suppression was detected in the muscle, and, finally, the behavioral time of stopping was ~220 ms. This temporal cascade supports a physiological model of action-stopping, and partitions it into subprocesses that are isolable to different nodes and are more precise than the behavioral latency of stopping. Variation in these subprocesses, including at the single-trial level, could better explain individual differences in impulse control.

To compare the strength-duration (S-D) time constants of motor cortex structures activated by current pulses oriented posterior-anterior (PA) or anterior-posterior (AP) across the central sulcus. Motor threshold and input-output curve, along with motor evoked potential (MEP) latencies, of first dorsal interosseus were determined at pulse widths of 30, 60, and 120 μs using a controllable pulse parameter (cTMS) device, with the coil oriented PA or AP. These were used to estimate the S-D time constant and we compared with data for responses evoked by cTMS of the ulnar nerve at the elbow. The S-D time constant with PA was shorter than for AP stimulation (230.9 ± 97.2 vs. 294.2 ± 90.9 μs; p<0.001). These values were similar to those calculated after stimulation of ulnar nerve (197 ± 47 μs). MEP latencies to AP, but not PA stimulation were affected by pulse width, showing longer latencies following short duration stimuli. PA and AP stimuli appear to activate the axons of neurons with different time constants. Short duration AP pulses are more selective than longer pulses in recruiting longer latency corticospinal output. More selective stimulation of neural elements may be achieved by manipulating pulse width and orientation.

Previous research suggested that anterior-posterior (AP) directed currents induced by TMS in motor cortex (M1) activate interneuron circuits different from those activated by posterior-anterior currents (PA). The present experiments provide evidence that pulse duration also determines the activation of specific interneuron circuits. To use single motor unit (SMU) recordings to confirm the difference in onset latencies of motor-evoked potentials (MEPs) evoked by different current directions and pulse durations: AP30, AP120, PA30 and PA120. To test whether the amplitude of the MEPs is differentially influenced by somatosensory inputs from the hand (short-latency afferent inhibition, SAI), and examine the sensitivity of SAI to changes in cerebellar excitability produced by direct current stimulation (tDCSCb). Surface electromyograms and SMUs were recorded from the first dorsal interosseous muscle. SAI was tested with an electrical stimulus to median or digital nerves ~20-25 ms prior to TMS delivered over the M1 hand area via a controllable pulse parameter TMS (cTMS) device. SAI was also tested during the application of anodal or sham tDCSCb. Because TMS pulse specificity is greatest at low stimulus intensities, most experiments were conducted with weak voluntary contraction to reduce stimulus threshold. AP30 currents recruited the longest latency SMU and surface MEP responses. During contraction SAI was greater for AP30 responses versus all other pulses. Online anodal tDCSCb reduced SAI for the AP30 currents only. AP30 currents activate an interneuron circuit with functional properties different from those activated by other pulse types. Pulse duration and current direction determine what is activated in M1 with TMS.