Abstract

BackgroundThe nerve fibre circuits around a lesion play a major role in the spontaneous recovery process after spinal cord hemisection in rats. The aim of the present study was to answer the following question: in the re-control process, do all spinal cord nerves below the lesion site participate, or do the spinal cord nerves of only one vertebral segment have a role in repair?MethodsFirst we made a T7 spinal cord hemisection in 50 rats. Eight weeks later, they were divided into three groups based on distinct second operations at T7: ipsilateral hemisection operation, contralateral hemisection, or transection. We then tested recovery of hindlimbs for another eight weeks. The first step was to confirm the lesion had role or not in the spontaneous recovery process. Secondly, we performed T7 spinal cord hemisections in 125 rats. Eight weeks later, we performed a second single hemisection on the ipsilateral side at T8–T12 and then tested hindlimb recovery for another six weeks.ResultsIn the first part, the Basso, Beattie, Bresnahan (BBB) scores and the electrophysiology tests of both hindlimbs weren’t significantly different after the second hemisection of the ipsilateral side. In the second part, the closer the second hemisection was to T12, the more substantial the resulting impairment in BBB score tests and prolonged latency periods.ConclusionsThe nerve regeneration from the lesion area after hemisection has no effect on spontaneous recovery of the spinal cord. Repair is carried out by all vertebrae caudal and ipsilateral to the lesion, with T12 being most important.

Highlights

  • The brain is plastic, and mammals are capable of spontaneous recovery after spinal cord injury

  • In the second part of the study, we investigated the innervation of vertebrae downstream of the lesion site to determine if regenerated axons target single or multiple vertebrae

  • We found that, after the spinal cord transection operation Motor-evoked potential (MEP) activities were still observed at the body surface

Read more

Summary

Introduction

The brain is plastic, and mammals are capable of spontaneous recovery after spinal cord injury. When the rats were subjected to the T7 and T12 hemisection at the same time, both hindlimbs instantly lost all movement (Courtine et al, 2008) This observation demonstrates that nerve fibers around the lesion participate in repair. These fibers must originate rostral to the lesion on the ipsilateral side, cross the midline to the contralateral side, travel down the spinal cord, and re-cross the midline caudal to the lesion (Ballermann & Fouad, 2006; Courtine et al, 2008; Etlin et al, 2010; Reed, Shum-Siu & Magnuson, 2008) These two different repair mechanisms are in conflict with each other, and further research is needed to confirm and explain the repair process. Repair is carried out by all vertebrae caudal and ipsilateral to the lesion, with T12 being most important

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call