Attempted endogenous tissue repair following experimental spinal cord injury in the rat: involvement of cell adhesion molecules L1 and NCAM?
Version of Record online: 24 DEC 2001
© Federation of European Neuroscience Societies
European Journal of Neuroscience
Volume 12, Issue 9, pages 3224–3238, September 2000
How to Cite
Brook, G. A., Houweling, D. A., Gieling, R. G., Hermanns, T., Joosten, E. A. J., Bär, D. P. R., Gispen, W.-H., Schmitt, A. B., Leprince, P., Noth, J. and Nacimiento, W. (2000), Attempted endogenous tissue repair following experimental spinal cord injury in the rat: involvement of cell adhesion molecules L1 and NCAM?. European Journal of Neuroscience, 12: 3224–3238. doi: 10.1046/j.1460-9568.2000.00228.x
- Issue online: 24 DEC 2001
- Version of Record online: 24 DEC 2001
- Received 12 May 2000, accepted 13 June 2000
- traumatic injury
It is widely accepted that the devastating consequences of spinal cord injury are due to the failure of lesioned CNS axons to regenerate. The current study of the spontaneous tissue repair processes following dorsal hemisection of the adult rat spinal cord demonstrates a phase of rapid and substantial nerve fibre in-growth into the lesion that was derived largely from both rostral and caudal spinal tissues. The response was characterized by increasing numbers of axons traversing the clearly defined interface between the lesion and the adjacent intact spinal cord, beginning by 5 days post operation (p.o.). Having penetrated the lesion, axons became associated with a framework of NGFr-positive non-neuronal cells (Schwann cells and leptomeningeal cells). Surprisingly few of these axons were derived from CGRP- or SP-immunoreactive dorsal root ganglion neurons. At the longest survival time (56 days p.o.), there was a marked shift in the overall orientation of fibres from a largely rostro-caudal to a dorso-ventral axis. Attempts to identify which recognition molecules may be important for these re-organizational processes during attempted tissue repair demonstrated the widespread and intense expression of the cell adhesion molecules (CAM) L1 and N-CAM. Double immunofluorescence suggested that both Schwann cells and leptomeningeal cells contributed to the pattern of CAM expression associated with the cellular framework within the lesion.