Abstract
Recent results have shown that exercise training promotes the recovery of injured rat distal spinal cords, but are still unclear about the function of skeletal muscle in this process. Herein, rats with incomplete thoracic (T10) spinal cord injuries (SCI) with a dual spinal lesion model were subjected to four weeks of treadmill training and then were treated with complete spinal transection at T8. We found that treadmill training allowed the retention of hind limb motor function after incomplete SCI, even with a heavy load after complete spinal transection. Moreover, treadmill training alleviated the secondary injury in distal lumbar spinal motor neurons, and enhanced BDNF/TrkB expression in the lumbar spinal cord. To discover the influence of skeletal muscle contractile activity on motor function and gene expression, we adopted botulinum toxin A (BTX-A) to block the neuromuscular activity of the rat gastrocnemius muscle. BTX-A treatment inhibited the effects of treadmill training on motor function and BDNF/TrKB expression. These results indicated that treadmill training through the skeletal muscle-motor nerve-spinal cord retrograde pathway regulated neuralplasticity in the mammalian central nervous system, which induced the expression of related neurotrophins and promoted motor function recovery.
Highlights
Spinal cord injury (SCI) is a severe traumatic condition of the central nervous system (CNS), which leads to movement deficiency, sensory and autonomic nerve dysfunction, and severely influences the quality of life of the patient (Lu et al, 2012)
Two days after complete spinal transection, motor function was completely lost in the sham group, and only a few joints of the hind legs could be moved in the SCI group (2.64 ± 1.03)
The results of this study showed that the functional changes in the lumbar spinal cord play an important role in the recovery of SCI in rats after treadmill training based on the dual spinal lesion model
Summary
Spinal cord injury (SCI) is a severe traumatic condition of the central nervous system (CNS), which leads to movement deficiency, sensory and autonomic nerve dysfunction, and severely influences the quality of life of the patient (Lu et al, 2012). How to cite this article Wu et al (2016), Neuromuscular interaction is required for neurotrophins-mediated locomotor recovery following treadmill training in rat spinal cord injury. Many studies have confirmed that exercise training can improve the recovery of locomotor function after SCI. Previous studies mainly focus on the changes at the SCI site per se, but the molecular and cellular process of the neuromuscular interaction by exercise training in spinal cord recovery has not been investigated yet. Exercise training can induce morphological and molecular changes in the distal spinal cord after SCI. Petruska et al (2007) found that exercise training can increase the number of nerve fibers in the white matter of the lumbar spinal cord after incomplete spinal cord injury (iSCI) in a rat model. Beaumont et al (2004) found that exercise training can improve secondary neuroprotenial abnormality of distal motor neurons after SCI Exercise training can induce morphological and molecular changes in the distal spinal cord after SCI. Petruska et al (2007) found that exercise training can increase the number of nerve fibers in the white matter of the lumbar spinal cord after incomplete spinal cord injury (iSCI) in a rat model. Beaumont et al (2004) found that exercise training can improve secondary neuroprotenial abnormality of distal motor neurons after SCI
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