The early stages of Wallerian degeneration in the severed optic nerve of the newt (Triturus viridescens).

Abstract

The initiation of Wallerian degeneration in the severed optic nerve of the newt (Triturus viridescens) was very rapid and intense. Significant degeneration of nonmyelinated axons was observed as early as six hours after lesion (h.a.l.) and was almost complete by 48 h.a.l. Initial degeneration of non-myelinated axons began in "extracellular digestion chambers" formed between burgeoning ependymoglial processes. The remaining fragments and debris were later phagocytized by surrounding ependymoglial processes. Many axons of myelinated fibers have degenerated as early as 6 h.a.l. However, the overall population of myelinated axons degenerates at a much slower rate than nonmyelinated ones, for many of them appear intact as late as 48 h.a.l. Some myelin sheaths show significant signs of degeneration by 6 h.a.l. Indeed, by this time a number of myelinated fibers have completely degenerated leaving only large vacuolated spaces in the nerve parenchyma. Swelling and vacuolization of the sheath are among the earliest signs of myelin degeneration. The ependymoglial cell response to optic nerve lesion is manyfold and dramatic. By 6 h.a.l. there are signs of burgeoning ependymoglial processes which begin to resemble scar formation (gliosis) by 48 h.a.l. The morphological evidence is consistent with the concept of an important phagocytic role of ependymoglial cells during the early stages of optic nerve degeneration.