Zhang, Yi; (1996) The expression and distribution of neural cell adhesion and extracellular matrix molecules after injury to, and peripheral nerve grafting into, the adult mammalian CNS. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

This study focuses on possible involvement of the neural cell adhesion molecules. N-CAM, polysialylated N-CAM (PSA) and L1, and the extracellular matrix molecule tenascin-C in the responses of CNS tissue to injury and the implantation of peripheral nerve autografts in adult rats by using immunohistochemistry (LM/EM) and in situ hybridization methods. After peripheral nerve grafts were inserted into the thalamus, Schwann cells up-regulated the expression of N-CAM, L1 and tenascin-C, regenerating thalamic axons in the graft became coated with PSA. N-CAM and L1. and L1 mRNA was selectively up-regulated in the neurons of the thalamic reticular nucleus which are the major source of regenerating axons in the grafts. Re-expression of the highly developmentally regulated PSA indicates that the regenerating axons reacquire characteristics of developing axons and the up-regulation of N-CAM, and especially L1, by regenerating CNS neurons suggests roles for these molecules in cellular interactions during axonal regeneration. However, regeneration of axons within the CNS was not consistently enhanced in transgenic mice with an L1 transgene under the control of the GFAP promoter. Regenerating thalamic axons (unlike regenerating sciatic axons in situ) also acquire a coating of tenascin-C, suggesting that they express a receptor able to bind graft-derived tenascin-C. After injury, tenascin-C is strongly up-regulated in the sciatic nerve and in the dorsal roots (where axonal regeneration occurs) and in the dorsal columns (where axonal regeneration does not normally occur). The few sprouts produced after dorsal column injury are found close to and within areas of high tenascin immunoreactivity. Thus tenascin-C is probably not responsible for inhibiting axon growth into, or within the spinal cord or along nerve grafts. A study of the pattern of expression and distribution of tenascin-C during postnatal development of the rat spinal cord was also made; tenascin-C expression by astrocytes was progressively down-regulated with development as expected, but unexpectedly, from postnatal day 7 onwards, a population of tenascin-C synthesising neurons was identified in the lumbar ventral horn.

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