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. 2004 Mar 3;24(9):2143–2155. doi: 10.1523/JNEUROSCI.3547-03.2004

Figure 3.

Figure 3.

Transgenically targeted ablation of reactive scar-forming astrocytes adjacent to stab SCI. A-G, J, I, Transverse sections of upper lumbar spinal cord after longitudinal stab SCI (arrowheads) in nontransgenic mice given GCV (A, E; NT+GCV), a GFAP-TK transgenic mouse not given GCV (C; Tg no GCV), or GFAP-TK transgenic mice given GCV (B, D, F, G, J, I; Tg+GCV). A-F, Single immunohistochemical staining for GFAP (A, B), TK (C, D), or BrdU (E, F) viewed by bright-field microscopy. G, I, J, Double immunohistochemical staining for GFAP and BrdU (G) or CD45 and BrdU (I, J) viewed by laser-scanning confocal microscopy. After stab SCI in control mice (A, C, E), astrocytes along the wound margin hypertrophy, upregulate their expression of GFAP (A) and TK (C), and take up BrdU. After stab SCI in transgenic mice given GCV for 7 d (B, D, F), GFAP- and TK-expressing astrocytes (B, D) and BrdU-labeled dividing cells (F) are substantially depleted from a large area around the center of the stab wound. Within this area, only GFAP-positive fragments of astrocytes remain (B, G, arrows). Astrocytes at the borders of this area have upregulated GFAP or TK during the 7 d after GCV delivery (B, D). Some dividing cells are present in the area depleted of astrocytes (F); all of these cells were GFAP-negative (G, arrowheads), and most were positive for the inflammatory cell marker CD45 (I, J). H, Graph showing mean ± SEM number of TK-positive cells within the 300 μm wound margin adjacent to the stab injury (see Fig. 1 D) in GFAP-TK transgenic mice not given GCV (Tg-GCV) or given GCV (Tg+GCV); n = 4 per group. **Significantly different from control, p < 0.01 (t test). Scale bars: A-F, 100 μm; G, 15 μm; J, 10 μm; I, 5 μm.