Abstract
The origin of the remyelinating oligodendrocyte in a focal antigalactocerebroside-induced demyelinating lesion of the cat optic nerve was studied with detailed correlative electron microscopy and immunocytochemistry using a panel of antigenic markers. Within 10 days of the destruction of all endogenous oligodendrocytes and demyelination of all axons in the lesion, a new population of small glial cells appeared coincident with division of the residual astrocytes and developed a process-bearing axon-embracing morphology. The processes of these small glial cells (SGCs) contained intermediate filaments composed not of glial fibrillary acidic protein but of vimentin and over the ensuing 14 days these cells confirmed their oligodendrocyte destiny by differentiating to lose the intermediate filaments, form myelin and acquire the acquire the typical oligodendrocyte antigenic phenotype. It is suggested that the extensive remyelination of this lesion is sponsored by the new population of SGCs which in turn are generated either by dedifferentiated reactive astrocytes or by as yet unidentified precursor cells.
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