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. 2015 Aug 6;63(12):2340–2361. doi: 10.1002/glia.22898

Figure 1.

Figure 1

Characterization of astrocytes in the intact and injured somatosensory cortex. (A) Fluorescence micrographs of GFP immunoreactivity in the intact somatosensory cortex of hGFAP‐eGFP mice at postnatal day (P65). Note that GFP is limited to few subpial astrocytes in the cortical layer I (LI) or parenchymal astrocytes in the vicinity of blood vessels (BV) in the intact cerebral cortex (Ctx). (B) After stab wound injury of hGFAP‐eGFP mice of the same age, GFP was found in virtually all GFAP+ reactive astrocytes including proliferating (Ki67+) reactive astrocytes (white arrowheads in B′). (C) Fluorescence micrographs depict representative confocal images of GFP immunostaining in the intact cerebral cortex (upper panel) of Aldh1L1eGFP transgenic mice. Double‐immunopositive cells for the calcium binding protein S100β in the intact gray matter (GM) and GFAP in the intact corpus callosum (CC), striatum (Str) and subependymal layer of lateral ventricle (LV) (lower panel). (D) Stab wound injury of Aldh1L1eGFP somatosensory GM induces a broad expression of GFAP in many (white arrowhead), but not all GM astrocytes (red arrowheads) at the injury site (D′). (E) Histogram depicting the number of the hGFAP‐GFP+ astrocytes in the penumbra of the injury increasing significantly over the first 7 dpi. (F) Fluorescence micrograph shows labeling for the DNA base analog BrdU (given ×1 i.p. 2 h before immunohistological processing) in GFP+ and GFAP+ astrocytes 5 dpi in hGFAP‐eGFP mouse cerebral cortex GM. (G) Quantification of the number of such cells is shown in the histogram with a significant increase within the first 5 dpi. All data are plotted as mean ± SEM from n = 5 experiments. Significance between means was analyzed using of one‐way ANOVA test and indicated as *(P < 0.05), **(P < 0.01), ***(P < 0.001). Scale bars: (A–D) 100 μm, (A′) 50 μm, (B′, D′) 25 μm, (A″, F) 10 μm.