Attempted endogenous tissue repair following experimental spinal cord injury in the rat: involvement of cell adhesion molecules L1 and NCAM?

It is widely accepted that the devastating consequences of spinal cord inju ry are due to the failure of lesioned CNS axons to regenerate. The current study of the spontaneous tissue repair processes following dorsal hemisecti on of the adult rat spinal cord demonstrates a phase of rapid and substanti al nerve fibre in-growth into the lesion that was derived largely from both rostral and caudal spinal tissues. The response was characterized by incre asing numbers of axons traversing the clearly defined interlace between the lesion and the adjacent intact spinal cord, beginning by 5 days post opera tion (p.o.). Having penetrated the lesion, axons became associated with a f ramework of NGFr-positive non-neuronal cells (Schwann cells and leptomening eal cells). Surprisingly few of these axons were derived from CGRP- or SP-i mmunoreactive dorsal root ganglion neurons. At the longest survival time (5 6 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 p rocesses during attempted tissue repair demonstrated the widespread and int ense expression of the cell adhesion molecules (CAM) L1 and N-CAM. Double i mmunofluorescence suggested that both Schwann cells and leptomeningeal cell s contributed to the pattern of CAM expression associated with the cellular framework within the lesion.