Cytoskeletal disruption following contusion injury to the rat spinal cord

Shu Xin Zhang, Mark Underwood, Alex Landfield, Feng Fa Huang, Sam Gibson, James W. Geddes

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Following experimental spinal cord injury (SCI), there is a delayed loss of neurofilament proteins but relatively little is known regarding the status of other cytoskeletal elements. The purpose of the present study was to compare the extent and time course of the MAP2 loss with that of neurofilament proteins, and to examine tau protein levels and distribution following SCI. Within 1 to 6 hours following SCI, there is rapid loss of MAP2, tau, and nonphosphorylated neurofilament proteins at the injury site. In contrast, the loss of phosphorylated neurofilament proteins was not significant until 1 week postinjury. In addition to the loss of MAP2 protein, there was extensive beading of MAP2-immunoreactive dendrites extending into the white matter. This was most pronounced 1 hour after injury and gradually resolved such that beading was no longer evident 2 weeks after SCI. The time course of beading resolution is similar to that of behavioral recovery following SCI, but the functional significance of the beading remains to be determined. Together, these results demonstrate that there are 2 phases of cytoskeletal disruption following SCI; a rapid loss of MAP2, tau, and nonphosphorylated neurofilament proteins, and a delayed loss of phosphorylated neurofilaments.

Original languageEnglish
Pages (from-to)287-296
Number of pages10
JournalJournal of Neuropathology and Experimental Neurology
Issue number4
StatePublished - Apr 2000


  • Dendrites
  • Microtubule-associated proteins
  • Neurofilament proteins
  • Tau proteins

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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