Stab wound lesion to the adult central nervous system induces strong proliferative response that is followed by the formation of a dense astroglial
scar. In order to determine the origin of those astrocytes composing the
glial scar, the cell proliferation marker
bromodeoxyuridine (
BrdU) was administered to lesioned rats that were fixed 3 h or 6 days later. At 3 h after the
BrdU administration, labeled nuclei were frequently associated with either NG2(+) cells or microglia/macrophages, but rarely with astrocytes expressing
glial fibrillary acidic protein (GFAP). Six days later, by contrast, numerous
BrdU-labeled nuclei were associated with astrocytes located along the lesion borders. After the injection of a viral vector of the
green fluorescent protein (GFP) into the lesional cavity, GFP was preferentially detected within NG2- or GFAP-labeled cells when lesioned animals were fixed 1 or 6 days after the
injections, respectively. The combined detection of glial markers within cells present in the lesioned area indicated that, although they rarely express GFAP, the marker of mature astrocytes, NG2(+) cells located along the lesion borders frequently express
nestin and
vimentin, i.e., two markers of immature astrocytes. Lastly, chronic treatment of lesioned rats with
dexamethasone was found to inhibit the proliferation of NG2(+) cells present within the lesioned area and to subsequently alter the formation of a dense astroglial
scar. Taken together, these data strongly suggest that following a surgical lesion, at least a portion of the astrocytes that constitute the
glial scar are issued from resident NG2(+) cells.