Dataset of analysed data from the article "Disrupted Inhibitory–Excitatory Balance Underlies Spinal Motoneuron Dysfunction in Incomplete Spinal cord Injury"

Incomplete spinal cord injury disrupts voluntary movement, in part through motoneuron dysfunction, yet the mechanisms underlying this dysfunction remain poorly understood. Using a non-invasive approach to decode the spiking activity of large populations of spinal motoneurons, we quantified the relative contributions of excitatory, inhibitory, and neuromodulatory inputs to motoneuron rate coding after chronic incomplete spinal cord injury. Eighteen participants with incomplete spinal cord injury and 18 age- and sex-matched control participants performed submaximal isometric plantar flexion tasks while high-density surface electromyography was recorded from the soleus and gastrocnemius medialis muscles. Motoneuron firing behaviour was analysed to estimate neuromodulatory drive and the balance between inhibitory and excitatory inputs. Participants with incomplete spinal cord injury exhibited lower rate coding, characterised by lower firing rates at recruitment, lower firing rate modulation, and lower peak firing rates compared with healthy controls. Although estimates of neuromodulatory drive did not differ between groups, individuals with spinal cord injury showed a shift in the inhibition-excitation balance toward greater inhibition compared with controls. Furthermore, increasing inhibitory input through muscle length changes and antagonist tendon vibration modulated motoneuron firing in controls, but not in individuals with incomplete spinal cord injury. Together, these findings suggest that impaired rate coding after incomplete spinal cord injury arises from an altered inhibitory-excitatory balance rather than reduced neuromodulatory drive. Taking advantage of methodological advances to decode spinal motor neuron activity during voluntary contraction, this study identified excessive inhibitory input to spinal motoneurons as a key neural mechanism contributing to muscle weakness and impaired motor function in individuals with incomplete spinal cord injury.