Electrical spinal cord stimulation enables paraplegic patients to regain voluntary leg movement. This treatment was only intended to engage local spinal networks to facilitate basic standing and postural stabilization without… Click to show full abstract
Electrical spinal cord stimulation enables paraplegic patients to regain voluntary leg movement. This treatment was only intended to engage local spinal networks to facilitate basic standing and postural stabilization without supraspinal input. Therefore the mechanism(s) enabling voluntary movement are unknown. Here we developed the first conditioned behavioral paradigm in rats for studying the recovery of voluntary movement after a paralyzing spinal injury and characterize the recovered neural connection. Rats were trained to kick their right hindlimb in response to an auditory cue. The rats then received a mid-thoracic spinal cord injury, causing hindlimb paralysis. After which, the rats were treated with spinal electro-neuromodulation across the lumbosacral enlargement. Two months after injury, spinal electro-neuromodulation enabled the rats to recover the trained behavior. Stopping or starting the electro-neuromodulation immediately abolished or facilitated recovery. Quipazine (nonspecific 5HT agonist) selectively abolished this recovered voluntary movement. Our work demonstrates a previously unknown highly specific reorganization phenomenon that can functionally reconnect the most distant neural structures. The interference of quipazine suggests the recovery mechanisms differ from those traditionally studied using electro-neuromodulation to recover postural and locomotor functions, and the speed of recovery of this conditioned behavior when electro-neuromodulation was applied proves these mechanisms are engaged within seconds of treatment.
               
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