Literature DB >> 2746287

Central axons in injured cat spinal cord recover electrophysiological function following remyelination by Schwann cells.

A R Blight1, W Young.   

Abstract

Axonal morphometry of the lesion site was studied at 3 months after standardized weight-drop contusion injury of the thoracic spinal cord in adult cats. From a sample of 25 injured animals, 12 examples were found in which all surviving axons in the dorsal column were remyelinated by Schwann cells, at the level of the lesion. The dorsolateral tracts were also peripherally myelinated in 6 of these cases, and there was no central myelination in complete transverse sections through the lesion in four animals. In these cases, Schwann cell myelination was prevalent for several millimeters on either side of the lesion center. The extent of Schwann cell invasion correlated with the intensity of injury, measured by overall axon loss. Cortical somatosensory evoked potentials (CSEP) were recorded from all animals before and at intervals for 12 weeks after injury. CSEP to hindlimb (tibial nerve) stimulation were lost immediately at injury but some recovery took place during the first month. The extent of CSEP recovery correlated negatively but weakly with overall axon loss. Clear SEP were recorded at 3 months post-injury in 3 of the animals in which the dorsal columns were remyelinated by Schwann cells; in one of these, the dorsolateral funiculi were also peripherally myelinated. In another, oligodendrocyte myelination was absent from the entire transverse section of the lesion site. Thus, abnormal remyelination by cells of the peripheral nervous system, which is known to occur in a variety of central demyelinating conditions, is capable of restoring effective action potential conduction in mammalian spinal cord sensory tracts.

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Year:  1989        PMID: 2746287     DOI: 10.1016/0022-510x(89)90073-7

Source DB:  PubMed          Journal:  J Neurol Sci        ISSN: 0022-510X            Impact factor:   3.181


  39 in total

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Review 7.  Cell transplantation therapy for spinal cord injury.

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8.  A selective glial barrier at motor axon exit points prevents oligodendrocyte migration from the spinal cord.

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9.  Cervical spinal demyelination with ethidium bromide impairs respiratory (phrenic) activity and forelimb motor behavior in rats.

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10.  Safety of human neural stem cell transplantation in chronic spinal cord injury.

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