Biology subjects

Escalante, Y.

Publications and source records attributed to Escalante, Y..

3 recordsLinked to original sources

bioRxiv2025

Dissociable Roles of Primary Motor and Supplementary Motor Cortex in Shaping the Neural Drive to Muscle

The primary motor cortex (M1) and supplementary motor area (SMA) are critical for motor execution and planning, yet their distinct causal contributions to modulating the neural drive to muscles remain incompletely understood. To dissociate their roles, we applied inhibitory transcranial magnetic stimulation (TMS) over M1, SMA, or a sham condition in 72 healthy participants and characterized the activity of single motor units from high-density EMG recorded during a sustained isometric contraction. Our results revealed a clear functional divergence. M1 inhibition produced a direct failure of motor output, causing a rapid force decline compared to sham, which was strongly correlated with a reduction in motor unit firing rates. Conversely, SMA inhibition did not impair net force. Instead, it altered the fundamental structure of the motor command, compelling a compensatory strategy characterized by a reliance on smaller-amplitude motor units with lower firing rates and a marked degradation of the low-frequency (delta-band) coherence that organizes stable output. These results provide direct causal evidence that M1 directly dictates the magnitude of motor output via population firing rates, while SMA orchestrates the composition and temporal structure of the active motor unit pool to generate an efficient and stable command. Significance StatementUsing causal brain stimulation, we provide the first direct evidence that the primary motor cortex (M1) and supplementary motor area (SMA) serve distinct, non-redundant roles in controlling motor unit populations. We show that inhibiting M1 directly impairs force magnitude by reducing motor unit firing rates. In contrast, inhibiting SMA spares net force but disrupts the underlying motor plan, compelling a compensatory strategy that uses smaller motor units and degrades temporal firing organization via a loss of delta-band coherence. By demonstrating that M1 governs motor power while SMA organizes motor strategy, this study opens new avenues for personalizing neuro-rehabilitation to address the specific cortical origin of a patients motor deficits.

neuroscience↗

bioRxiv2025

Changes in Motor Unit Activity of Co-activated Muscles During Dynamic Force Field Adaptation

Muscle co-contraction plays a critical role in motor adaptation by minimizing movement errors and enhancing joint stability in novel dynamic environments. However, the underlying changes in motor unit (MU) activity within co-activated muscles during adaptation remain largely unexplored. To investigate this, we employed advanced electromyography sensor arrays and signal processing to examine MU activation in the triceps brachii (agonist) and biceps brachii (antagonist) during a reaching task under force-field perturbation. Our results revealed a gradual reduction in movement errors and an increase in velocity with adaptation, accompanied by a decrease in muscle co-contraction from early to late adaptation phases. This reduction was primarily driven by increased triceps activity, while biceps activity remained unchanged throughout the adaptation process. At the MU level, recruitment, amplitude, and firing rate increased in both muscles during adaptation compared to baseline (without force-field perturbation). However, from early to late adaptation phases, triceps MU amplitude continued to increase, while its firing rate stabilized, suggesting a shift in force generation strategy. In contrast, biceps MU activity remained stable throughout the adaptation. These findings indicate that the reduction in co-contraction during motor adaptation is likely mediated by a shift in motor unit control strategy within the agonist muscle. The increased reliance on MU amplitude modulation rather than firing rate in later adaptation may represent a mechanism for optimizing force production while maintaining movement accuracy and joint stability in dynamic environments. NEW & NOTEWORTHYThis study examines how motor unit (MU) activity changes during motor adaptation in dynamic environments. We show that reduced co-contraction during adaptation is primarily driven by increased agonist MU amplitude rather than firing rate changes. In contrast, antagonist MU activity remains stable. These findings highlight a shift in MU control strategy that optimizes force production while maintaining movement accuracy, providing new insights into the underlying neuromuscular mechanisms of motor adaptation.

neuroscience↗

bioRxiv2023

Pathological brain states in Alzheimer's disease

Dynamic and rapid reconfigurations of neural activation patterns, known as brain states, support cognition. Recent analytic advances applied to functional magnetic resonance imaging now enable the quantification of brain states, which offers a substantial methodological improvement in characterizing spatiotemporal dynamics of activation over previous functional connectivity methods. Dysfunction to the persistence and temporal transitions between discrete brain states may be proximal factors reflecting neurophysiological disruptions in Alzheimers disease, although this has not yet been established. Here, we identified six distinct brain states, representing spatiotemporal trajectories of coactivation at single time points, in older adults across the Alzheimers disease continuum. Critically, we identified a pathological brain state that reflects coactivation within limbic regions. Higher persistence within and transitions to this limbic state, at the expense of other brain states, is associated with an increased likelihood of a clinically impaired diagnosis, worse cognitive performance, greater Alzheimers pathology, and neurodegeneration. Together, our results provide compelling evidence that neural activity settling into a pathological limbic state reflects the progression to Alzheimers disease. As brain states have recently been shown to be modifiable targets, this work may inform the development of novel neuromodulation techniques to reduce limbic state persistence. This application would be an innovative clinical approach to rescue cognitive decline in the early stages of Alzheimers disease.

neuroscience↗