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Journal of Neuroscience, Vol 16, 2064-2073, Copyright © 1996 by Society for Neuroscience
Glial cells are increased proportionally in transgenic optic nerves with increased numbers of axons
JF Burne, JK Staple and MC Raff
Medical Research Council Developmental Neurobiology Programme, MRC Laboratory for Molecular Cell Biology, University College London, United Kingdom.
To study how an increase in axon number influences the number of glial
cells in the mammalian optic nerve, we have analyzed a previously described
transgenic mouse that expresses the human bcl-2 gene from a neuron-specific
enolase promoter. In these mice, the normal postnatal loss of retinal
ganglion cell axons is greatly decreased and, as a consequence, the number
of axons in the optic nerve is increased by approximately 80% compared with
wild-type mice. Remarkably, the numbers of oligodendrocytes, astrocytes,
and microglial cells are all increased proportionally in the transgenic
optic nerve. The increase in oligodendrocytes apparently results from both
a decrease in normal oligodendrocyte death and an increase in
oligodendrocyte precursor cell proliferation, whereas the increase in
astrocytes apparently results from an increase in the proliferation of
astrocyte lineage cells. Unexpectedly, the transgene is expressed in
oligodendrocytes and astrocytes, but this does not seem to be responsible
for the increased numbers of these cells. These findings indicate that
developing neurons and glial cells can interact to adjust glial cell
numbers appropriately when neuronal numbers are increased. We also show
that the expression of the bcl-2 transgene in retinal ganglion cells
protects the cell body from programmed cell death when the axon is cut, but
it does not protect the isolated axon from Wallerian degeneration, even
though the transgene-encoded protein is present in the axon.
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