Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury

Area of Science:

• Neuroscience
• Spinal Cord Injury Research
• Motor Control

Background:

• Severe spinal cord injury (SCI) causes progressive neuronal dysfunction in humans, marked by muscle exhaustion during locomotion and abnormal reflexes.
• The chronic stage of SCI is associated with impaired motor function, suggesting underlying neural changes caudal to the injury site.

Purpose of the Study:

• To investigate the hypothesis that undirected compensatory plasticity in neural systems caudal to SCI contributes to chronic neuronal dysfunction.
• To evaluate functional, electrophysiological, and neuromorphological changes in lumbosacral circuitries following a thoracic hemisection injury in rats.

Main Methods:

• Adult rats underwent a staggered thoracic hemisection to induce SCI.
• Assessed functional locomotion, electrophysiology, and neuromorphology of spinal cord segments caudal to the injury.
• Analyzed circuit, fiber, and synapse density, alongside reflex responses and muscle activity.

Main Results:

• Rats displayed chronic neuronal dysfunction, including antagonistic muscle co-activation, locomotor muscle exhaustion, and gait deterioration.
• Abnormal, long-latency reflex responses in leg muscles were observed, mirroring human SCI.
• Extensive, lamina-specific remodeling of neural networks caudal to the SCI occurred, restoring synaptic input levels.

Conclusions:

• Undirected compensatory plasticity in spinal neurons aims to re-establish synaptic environments after loss of supraspinal input.
• This aberrant neural rewiring forms maladaptive circuits, leading to inappropriate sensorimotor network engagement during gait.
• The study links neuronal dysfunction, abnormal reflexes, and anatomical remodeling in the chronic phase of SCI.