Shota Tsugaya, Akihiro Nakamura, Taishin Nomura
Electroencephalographic (EEG) studies of human quiet stance demonstrate beta-band event-related desynchronization (beta-ERD) during the micro-fall phase of postural sway, followed by event-related synchronization (beta-ERS; post-movement beta rebound) during the micro-recovery phase. These modulations correlate with intermittent ankle muscle inactivation that exploits the stable manifolds of an unstable upright equilibrium; however, how such sway-related beta dynamics may arise within closed-loop brain-body interactions remains unclear. Here, we investigated a possible circuit-level account of these dynamics using an embodied spiking neural network model of the cortico-basal ganglia-thalamic (CBGT) circuitry integrated with an inverted pendulum. In this closed-loop system, continuous sensory feedback is integrated into the striatum, while the motor cortex executes decisions via drift-diffusion-like population competition, where the decision time (DT) represents the intermittent control-off period. We demonstrate that simulated cortical LFPs exhibit characteristic sway-phase-locked beta-ERD and beta-ERS when corticostriatal synaptic weights are functionally balanced to implement intermittent control. Conversely, a forced-choice continuous-like regime that ceaselessly generates feedback torque fails to replicate these modulations, sustaining flat network states devoid of control-off periods (DT). Structural dissections show that, within the model, disrupting bidirectional thalamocortical loops or the GPe-STN circuit abolishes sway-phase-locked beta modulation, despite continuous sensory drive. Our findings provide a computational account linking sway-phase-locked beta activity to intermittent motor selection within the proposed CBGT framework. This closed-loop modeling framework offers a testable candidate account for how alterations in brain-body dynamics may jointly affect behavioral intermittency and beta-band modulation, with potential relevance to postural impairments in clinical conditions such as Parkinson's disease.Significance Statement Intermittent motor commands during quiet standing are accompanied by phase-specific cortical beta-band modulations, but how these neural dynamics may relate to intermittent postural control remains unclear. Here, using a closed-loop model integrating spiking cortico-basal ganglia-thalamic (CBGT) circuitry with body dynamics, we show that human-like beta modulations arise when the model implements intermittent control. Within the model, these modulations are abolished by disrupting thalamocortical or GPe-STN interactions and are absent in a forced-choice continuous-like regime. These findings provide a computational account linking intermittent postural control to sway-related beta dynamics and identify circuit interactions sufficient for their emergence within the proposed CBGT framework. The model offers testable predictions for investigating how brain-body interactions shape beta dynamics in healthy and impaired postural control.