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Down‐regulation of GAP‐43 During Oligodendrocyte Development and Lack of Expression by Astrocytes In Vivo: Implications for Macroglial Differentiation
Author(s) -
Curtis Rory,
Hardy Rebecca,
Reynolds Richard,
Spruce Barbara A.,
Wilkin Graham P.
Publication year - 1991
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1991.tb00099.x
Subject(s) - oligodendrocyte , immunocytochemistry , progenitor cell , biology , in vivo , microbiology and biotechnology , astrocyte , neuroglia , progenitor , in vitro , neuroscience , central nervous system , stem cell , myelin , biochemistry , endocrinology , genetics
Abstract The discovery of molecular markers which are selectively expressed during the development of specific classes of rat central nervous system macroglia has greatly advanced our understanding of how these cells are related. In particular, it has been shown in tissue culture that oligodendrocytes and some astrocytes (type‐2) may be derived from a common progenitor cell (O‐2A progenitor). However, the existence of type‐2 astrocytes in vivo has yet to be unequivocally established. Recently, it has been reported that the neural‐specific growth‐associated protein‐43 (GAP‐43, otherwise known as 8–50, F1, pp46 and neuromodulin) may be expressed by cells of the O‐2A lineage in vitro. We set out to examine the cellular specificity of GAP‐43 in O‐2A progenitors and their descendants in vitro and in vivo. Using a polyclonal antiserum against a GAP‐43 fusion protein we have shown the presence of immunoreactive GAP‐43 in the membranes of bipotential O‐2A glial progenitor cells and type‐2 astrocytes by Western blotting and immunocytochemistry of cells in culture. In contrast to previous studies, double labelling with mature oligodendrocyte markers showed that GAP‐43 is down‐regulated during oligodendrocyte differentiation in vitro. Immunohistochemical staining of sections of developing rat brain demonstrated the same developmental regulation of GAP‐43, suggesting that oligodendrocytes only express GAP‐43 at immature stages. In addition, normal and reactive astrocytes in tissue sections were not labelled with GAP‐43.