Abstract
Spinal cord injury (SCI) often results in death of spinal neurons and atrophy of muscles which they govern. Thus, following SCI, reorganizing the lumbar spinal sensorimotor pathways is crucial to alleviate muscle atrophy. Tail nerve electrical stimulation (TANES) has been shown to activate the central pattern generator (CPG) and improve the locomotion recovery of spinal contused rats. Electroacupuncture (EA) is a traditional Chinese medical practice which has been proven to have a neural protective effect. Here, we examined the effects of TANES and EA on lumbar motor neurons and hindlimb muscle in spinal transected rats, respectively. From the third day postsurgery, rats in the TANES group were treated 5 times a week and those in the EA group were treated once every other day. Four weeks later, both TANES and EA showed a significant impact in promoting survival of lumbar motor neurons and expression of choline acetyltransferase (ChAT) and ameliorating atrophy of hindlimb muscle after SCI. Meanwhile, the expression of neurotrophin-3 (NT-3) in the same spinal cord segment was significantly increased. These findings suggest that TANES and EA can augment the expression of NT-3 in the lumbar spinal cord that appears to protect the motor neurons as well as alleviate muscle atrophy.
Highlights
Spinal cord injury (SCI) is a worldwide problem and causes immense suffering and burden to the patient
To determine the neuroprotection of Tail nerve electrical stimulation (TANES) or EA treatment, the survival of motor neurons (L3 and L5 segments) in the transected spinal cord was evaluated after the neutral red staining
The present study investigated whether TANES or EA treatment could protect motor neurons of the lumbar spinal cord controlling the muscles of the hindlimbs and whether they would alleviate the skeletal muscle atrophy after complete SCI
Summary
Spinal cord injury (SCI) is a worldwide problem and causes immense suffering and burden to the patient. Traumatic injuries to the spinal cord disrupt the transmission of both ascending sensory projections and descending projections to motor neurons, leading to permanent sensory and motor functional deficits [1]. The motor neurons in the ventral horn of the spinal cord below the lesion site retain their connection to the target muscles, the loss of ascending and descending stimulation makes the spinal motor neurons shrink and die, resulting in atrophy of the innervated muscles. Neural Plasticity hypotrophy after SCI, and this includes using physical exercises to drive the disused hindlimbs [4, 5] and giving a localized electrical stimulation to the atrophic muscles [6, 7]. It was thought that external intervention like locomotor training or functional electrical stimulation could provide sensory inputs and effectively reactivate the lumbar motor circuit, giving a rise to the neuromuscular activity
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