Task-specific modulation of corticospinal neuron activity during skilled motor learning

Abstract

The learning of motor skills relies on plasticity of the primary motor cortex as task acquisition drives the remodeling of cortical motor networks. Large scale cortical remodeling of evoked motor outputs occurs in response to the learning of skilled, corticospinal-dependent behavior, but not simple, unskilled tasks. Here we determine the response of corticospinal neurons to both skilled and unskilled motor training and assess the role of corticospinal neuron activity in the execution of the trained behaviors. Using in vivo calcium imaging, we found that refinement of corticospinal activity correlated with the development of skilled, but not unskilled, motor expertise. Animals that failed to learn our skilled task exhibited a limited repertoire of dynamic movements and a corresponding absence of network modulation. Transection of the corticospinal tract and aberrant activation of corticospinal neurons show the necessity for corticospinal network activity patterns in the execution of skilled, but not unskilled, movement. We reveal a critical role for corticospinal network modulation in the learning and execution of skilled motor movements. The integrity of the corticospinal tract is essential to the recovery of voluntary movement after central nervous system injuries and these findings should help to shape translational approaches to motor recovery.

Effects of noninvasive neuromodulation targeting the spinal cord on early learning of force control by the digits

“…= 0.02 N) across baseline time points without any difference between conditions. This finding was supported by a significant effect of PRELOAD (F(1,22) = 32.02, p < 0.001, η p 2 = 0.59) on RMSE, indicating that forces generated after lengthening contractions were less stable than those produced after shortening contractions. Mean RMSE values for the eccentric preload were relatively consistent at baseline across conditions (Rest = 0.339 ± 0.141 N; Sham = 0.359 ± 0.139 N; Active = 0.301 ± 0.115 N), ranging from 0.121 to 0.841 N across all subjects and time points.…”

“…21 One consideration as it pertains motor skill (re)acquisition is how neuromodulation targeting synapses linking descending motor commands onto the final common pathway might interact with task repetition to influence learning. Distinct patterns of temporal coding by corticospinal neurons underlie acquisition of task-specific limb movements in rodent models, 22 and invasive neuromodulatory strategies shown to enhance re-learning of functions compromised by neurological injury involve plasticity mechanisms unique to circuits engaged during task-specific behavior. 23 It therefore stands to reason that administering PCMS against the backdrop of taskspecific activity may have some effect on early motor skill learning in humans; at least in those who show an upregulation of corticospinal transmission with the same dose of stimulation.…”

Neuropathic pain in a chronic CNS injury model is mediated by CST-targeted spinal interneurons

“…Pyramidotomy was performed as previously described 12 . Briefly, mice were deeply anaesthetized with isoflurane, the fur was shaved, bupivacaine (5 mg/mL) was injected, and a 1cm incision was made over the ventral midline.…”

“…The corticospinal tract (CST) is a critical descending pathway for modulating dexterous motor control and afferent fiber inhibition [9][10][11] . Damage to the CST results in immediate loss of precise motor control [12][13][14] , and impairs behavioral responses to light touch and mechanical allodynia 15 . These multifaceted roles in control of both movement and sensory processing rely on its anatomical connections with distinct populations of interneurons within the spinal cord [16][17][18] .…”