The remyelinative capacity of the central nervous system was investigated in the superior cerebellar peduncles of mice chronically demyelinated for 6 to 7 months by the administration of Cuprizone. It was found that, although the axons retained their capacity for remyelination, this capacity was greatly reduced compared to acutely demyelinated animals. The possible causes for this reduction were examined, and it was concluded that the limiting factor was the decreased availability of oligodendrocytes for remyelination, rather than inherent factors in the axons, or changes in the surrounding glial environment. The implications for both experimental and clinical disease are discussed.
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