• S X Zhang, M Underwood, A Landfield, F F Huang, S Gison, and J W Geddes.
• Sanders-Brown Center on Aging, and the Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, USA.
• J. Neuropathol. Exp. Neurol. 2000 Apr 1;59(4):287-96.

AbstractFollowing 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.

24 keywords...

hide…