An α -MN collateral to γ -MNs can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.
Grace NiyoLama I AlmofeezAndrew ErwinFrancisco J Valero-CuevasPublished in: bioRxiv : the preprint server for biology (2023)
The primary motor cortex does not uniquely or directly produce α -MN drive to muscles during voluntary movement. Rather, α -MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening (antagonist) muscles, which are thought to be inhibited by the shortening (agonist) muscles. It remains an open question, however, the extent to which velocity-dependent stretch reflexes disrupt voluntary movement, and whether and how they are inhibited in limbs with numerous monoand multi-articular muscles where agonist and antagonist roles become unclear and can switch during a movement. We used a computational model of a Rhesus Macaque arm to simulate movements with feedforward α -MN commands only, and with added velocity-dependent stretch reflex feedback. We found that velocity-dependent stretch reflex caused movement-specific, typically large and variable disruptions to the arm endpoint trajectories. In contrast, these disruptions became small when the velocity-dependent stretch reflexes were simply scaled by the α -MN drive to each muscle (equivalent to an α -MN excitatory collateral to its homologous γ -MNs, but distinct from α - γ co-activation. We argue this circuitry is more neuroanatomically tenable, generalizable, and scalable than α - γ co-activation or movement-specific reciprocal inhibition. We propose that this mechanism at the homologous propriospinal level, by locally and automatically regulating the highly nonlinear neuro-musculo-skeletal mechanics of the limb, could be a critical low-level enabler of learning, adaptation, and performance via cerebellar and cortical mechanisms.