Journal of Neurocytology

, Volume 25, Issue 1, pp 465–480

Primary demyelination and regeneration of ascending axons in the dorsal funiculus of the rat spinal cord following photochemically induced injury

Authors

  • Natasha J. Olby
    • Department of Clinical Veterinary Medicine
  • William F. Blakemore
    • Department of Clinical Veterinary Medicine
Article

DOI: 10.1007/BF02284816

Cite this article as:
Olby, N.J. & Blakemore, W.F. J Neurocytol (1996) 25: 465. doi:10.1007/BF02284816

Summary

The extent of primary demyelination and regeneration of ascending axons in the dorsal funiculus of the rat spinal cord was investigated following photochemically-induced ischaemic injury. Groups of rats were killed at intervals from 48h to 1 month after injury and a combination of light and electron microscopy and counting of axons in specific sites was used to study the axonal changes. Unmyelinated axons were noted in the dorsal rim of the lesion at its centre and at the centre of the gracile fasciculus at the caudal end of the lesion 7 days after injury. By 1 month, axons in these sites were thinly myelinated by Schwann cells or oligodendrocytes. In order to differentiate between remyelination of demyelinated axons and myelination of regenerated axons, axon counts were performed. The number of sub-pial axons present at the lesion centre did not change significantly from 48h to 1 month after injury, whereas the number of axons at the caudal end of the lesion increased significantly from 4 to 10 days after injury. We therefore conclude that sub-pial axons at the lesion centre are demyelinated between 4 and 7 days after injury and subsequently remyelinated by Schwann cells. At the caudal end of the lesion, a specific population of small diameter axons located at the centre of the gracile fasciculus regenerates for a distance of approximately 1 mm between 4 and 10 days after injury; these axons are then myelinated by oligodendrocytes or Schwann cells. In contrast, larger diameter axons of the gracile fasciculus do not show a regenerative response, demonstrating the variability of axonal responses to injury.

Copyright information

© Chapman and Hall 1996