Intraorbital transection of the rabbit optic nerve: consequences for ganglion cells and neuroglia in the retina.

Rabbit retinae were stained with antibodies to glial fibrillary acidic protein (GFAP) at various times up to 5 months after complete unilateral intraorbital optic nerve transection, which is known to induce degeneration of ganglion cell axons and perikarya in the retina. A transient immunoreactivity for GFAP was observed in Müller glial cells that normally lack this marker. Müller-cell GFAP immunoreactivity became detectable 4 days after the lesion, but Müller cells were no longer labeled 3 months later. GFAP-labeled astrocytes located in the nerve fiber layer showed no change in immunoreactivity at any stage after transection. Application of horseradish peroxidase to the left and right superior colliculus of a rabbit whose optic nerve had been transected unilaterally 2 years before confirmed the completeness of the transection. Yet electron microscopy showed the presence of some healthy-looking ganglion cell axons in the lesioned retina, although these cells were deprived of their target. Labeling retinal wholemounts with neurofilament antibodies confirmed the presence of some ganglion cell axons and perikarya in the retina more than 2 years after transection. The course of these axons suggested that they were remnants of axons. Using antibodies to galactocerebroside (GC) we found that, as in the normal rabbit, these persisting ganglion cell axons were myelinated in the medullary rays. Although many ganglion cell axons had disappeared after 2 years, the number of neuroglial cells (including astrocytes and oligodendrocytes) present in the medullary ray region was not altered. The cell bodies of some oligodendrocytes were covered with a myelin sheath, an aberrant feature not seen normally.