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Glial cell loss, proliferation and replacement in the contused murine spinal cord
Author(s) -
Lytle Judith M.,
Wrathall Jean R.
Publication year - 2007
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.1460-9568.2007.05390.x
Subject(s) - microglia , progenitor cell , endogeny , genetically modified mouse , spinal cord injury , spinal cord , bromodeoxyuridine , neuroglia , biology , microbiology and biotechnology , transgene , oligodendrocyte , white matter , neuroscience , immunology , central nervous system , medicine , stem cell , endocrinology , inflammation , immunohistochemistry , myelin , genetics , gene , magnetic resonance imaging , radiology
Studies in the rat have shown that contusive spinal cord injury (SCI) results in devastating pathology, including significant loss of mature oligodendrocytes and astrocytes even in spared white matter. Subsequently, there is increased proliferation of endogenous NG2 + cells, postulated to contribute to replacement of mature glia chronically, which is important for functional recovery. Studies of mechanisms that stimulate endogenous progenitor cells would be facilitated by using mouse models with naturally occurring and genetically engineered mutations. To determine whether the murine response is similar to that in the rat, we performed contusive SCI on adult female C57Bl/6 mice at the T8–9 level. Animals received bromodeoxyuridine injections in the first week following injury and were killed at 1, 3, 4, 7 or 28 days postinjury (DPI). The overall loss of macroglia and the temporal–spatial response of NG2 + cells after SCI in the (C57Bl/6) mouse was very similar to that in the (Sprague–Dawley) rat. By 24 h after SCI nearly half of the macroglia in spared ventral white matter had been lost. Cell proliferation was increased at 1–7 DPI, peaking at 3–4 DPI. Dividing cells included NG2 + cells and Cd11b + macrophages and microglia. Furthermore, cells dividing in the first week expressed markers of mature glia at 28 DPI. The similarities in endogenous progenitor cell response to SCI in the mouse and rat suggest that this is a fundamental injury response, and that transgenic mouse models may be used to further probe how this cellular response to SCI might be enhanced to improve recovery after SCI.