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Poster Sessions CP08: Schwann Cells

In multiple sclerosis, demyelination may be associated with axonal damage, but the alterations of the axonal cytoskeleton are largely unknown, as well as their consequences on remyelination. In this study, therefore, we have analysed the remyelination, after lysophosphatidylcholine (LPC) stereotaxic injection, in the CNS of transgenic NFH-lacZ mice, which present axonal atrophy caused by abnormal distribution of neurofilaments (NF), associated with hypermyelination in the peripheral nervous system (PNS), and normal myelin thickness in the CNS. Axonal atrophy in the CNS of NFH-lacZ mice was confirmed, but it wasn’t worsened by LPC-induced demyelination. On the contrary, demyelination induced axonal atrophy in wild-type mice, demonstrating that NF are essential for axonal calibre determination. Moreover, an efficient spontaneous remyelination (without hypermyelination) occurred in NFH-lacZ as well as in wild-type mice, indicating that NF are not necessary for CNS remyelination. Nevertheless, the reasons for PNS axons hypermyelination in NFH-lacZ mice are unknown. Thus, after LPCinduced demyelination, we have analysed the capacity of NFH-lacZ Schwann cells (SC) grafts to remyelinate the CNS of wild-type and NFH-lacZ mice, in order to determine whether the extracellular environment of the CNS could prevent hypermyelination. Although NFH-lacZ SC showed a lower shortterm survival in vitro, they migrate and myelinate as well as wild-type SC in vivo. The higher percentage of hypermyelinated axons in NFH-lacZ mice grafted with wild-type SC, demonstrated that abnormal axons are responsible for SC hypermyelination restricted to SC and sparing oligodendrocytes, whereas NFH-lacZ SC grafted in wild-type mice did not produce aberrant myelination, indicating their correct functioning in the presence of NF.