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© The Rockefeller University Press, 0021-9525/1999//1365 $5.00
The Journal of Cell Biology, Volume 146, Number 6, , 1999 1365-1374

Original Article

Rat Optic Nerve Oligodendrocytes Develop in the Absence of Viable Retinal Ganglion Cell Axons



H. Uedaa, J.M. Levineb, R.H. Millerc, and B.D. Trappa

a Department of Neurosciences, The Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195
b Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794
c Department of Neuroscience, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106
Department of Neurosciences, NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195.(216) 444-7927(216) 444-7177

trappb{at}ccf.org

Retinal ganglion cell axons and axonal electrical activity have been considered essential for migration, proliferation, and survival of oligodendrocyte lineage cells in the optic nerve. To define axonal requirements during oligodendrogenesis, the developmental appearance of oligodendrocyte progenitors and oligodendrocytes were compared between normal and transected optic nerves. In the absence of viable axons, oligodendrocyte precursors migrated along the length of the nerve and subsequently multiplied and differentiated into myelin basic protein–positive oligodendrocytes at similar densities and with similar temporal and spatial patterns as in control nerves. Since transected optic nerves failed to grow radially, the number of oligodendrocyte lineage cells was reduced compared with control nerves. However, the mitotic indices of progenitors and the percentage of oligodendrocytes undergoing programmed cell death were similar in control and transected optic nerves. Oligodendrocytes lacked their normal longitudinal orientation, developed fewer, shorter processes, and failed to form myelin in the transected nerves. These data indicate that normal densities of oligodendrocytes can develop in the absence of viable retinal ganglion axons, and support the possibility that axons assure their own myelination by regulating the number of myelin internodes formed by individual oligodendrocytes.

Key Words: oligodendrocyte progenitor cells • axon–glial interactions • myelination • optic nerve • program cell death

© 1999 The Rockefeller University Press

1.used in this paper: BrdU, bromodeoxyuridine; MBP, myelin basic protein; OPC, oligodendrocyte progenitor cell; PCD, programmed cell death


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