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The fine structure of pulse labeled ( 3 H‐thymidine cells) in degenerating rat optic nerve
Author(s) -
Skoff Robert P.
Publication year - 1975
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.901610408
Subject(s) - enucleation , wallerian degeneration , biology , optic nerve , thymidine , neuroglia , pathology , population , microglia , microbiology and biotechnology , precursor cell , cell , anatomy , neuroscience , central nervous system , immunology , biochemistry , in vitro , medicine , genetics , demography , sociology , inflammation
The ultrastructure of pulse labeled ( 3 H‐thymidine) cells in rat optic nerve undergoing Wallerian degeneration is described. The study was limited to the first ten days after enucleation since cell proliferation during this interval is greater than in normal optic nerve (Skoff and Vaughn, '71). Approximately one‐third of the pulse labeled cells are astrocytes. The majority of the proliferating astrocytes are in a reactive state, having changed their normal fibrous appearance to one showing a paucity of filaments. Thirty percent of the pulsed cells can be classified as microglia. Only immature oligodendrocytes proliferate, and they account for less than 10% of the pulse labeled cells. About 30% of the labeled population are undifferentiated glial precursor cells. Electron microscopic autoradiographic data obtained from normal optic nerve and presented in this paper indicates that glial precursor cells which have divided shortly before enucleation continue to proliferate after it. The evidence suggests that recently formed glial precursor cells transform into phagocytes following enucleation. Less than 3% of the pulse labeled cells examined in this study are ultrastructurally similar to mononuclear leukocytes. The results of the present study together with previous studies of degenerating optic nerve indicate that most phagocytes in Wallerian degeneration are derived from proliferation of intrinsic glia rather than from an invasion of exogenous cells.