Disappearance of astrocytes and invasion of macrophages following crush injury of adult rodent optic nerves: implications for regeneration

Exp Neurol. 1992 Oct;118(1):105-15. doi: 10.1016/0014-4886(92)90027-n.


Injury to the mammalian central nervous system results in loss of function because of its inability to regenerate. It has been postulated that some axons in the mammalian central nervous system have the ability to regenerate but fail to do so because of the inhospitable nature of surrounding glial cells. For example, mature oligodendrocytes were shown to inhibit axonal growth, and astrocytes were shown to form scar tissue that is nonsupportive for growth. In the present study we report an additional phenomenon which might explain the failure of axons to elongate across the site of the injury, namely, the absence of astrocytes from the crush site between the glial scar and the distal stump. Astrocytes began to disappear from the injury site as early as 2 days after the injury. After 1 week the site was necrotic and contained very few glial cells and numerous macrophages. Disappearance of glial cells was demonstrated in both rabbit and rat optic nerves by light microscopy, using antibodies directed against glial fibrillary acidic protein, and by transmission electron microscopy. Results are discussed with reference to possible implications of the long-lasting absence of astrocytes from the injury site, especially in view of the differences between the present findings in rodents and our recent observations in fish.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / pathology*
  • Astrocytes / ultrastructure
  • Cell Count
  • Cell Movement
  • Immunohistochemistry
  • Macrophages / physiology*
  • Macrophages / ultrastructure
  • Microscopy, Electron
  • Nerve Crush
  • Nerve Regeneration*
  • Optic Nerve / pathology
  • Optic Nerve / ultrastructure
  • Optic Nerve Injuries*
  • Rabbits
  • Rats
  • Rats, Sprague-Dawley