Figure 3.
Differing patterns of reactive astrogliosis after mild and moderate traumatic brain injury (TBI). Reactive astrogliosis (glial fibrillary acidic protein (GFAP), red) and microgliosis (CD68, green) were evaluated after mild and moderate TBI. (A, C, G) Whole-slice montages demonstrate the extent of reactive gliosis in control animals and 3 days after TBI. (D–F) Within the cerebral cortex, reactive gliosis declines between 7 and 14 days after mild TBI. Control (no TBI) cortex exhibits little GFAP immunoreactivity (B). (H–J) After moderate TBI, cortical reactive gliosis does not resolve for more than 14 days post injury. (K-L) Quantification of reactive astrogliosis 3, 7, 14, and 28 days after TBI shows that astrogliosis after mild TBI is transient within both the ipsilateral cerebral cortex (K) and striatum (L), yet is more persistent after moderate TBI. Peak reactive gliosis at 7 days post injury does not significantly differ between mild and moderate injury. **P<0.01, ***P<0.001 ipsilateral vs. contralateral; #P<0.05 moderate vs. mild TBI; †P<0.05, ††P<0.01, †††P<0.001 between ipsilateral time points; ‡P<0.01 between contralateral time points (two-way analysis of variance (ANOVA)). (M–O) Post-traumatic reactive astrogliosis was evident in both the ipsilateral and contralateral hippocampus 7 days after both mild (N) and moderate (P) TBI. Hippocampal reactive astrogliosis persisted at least 28 days after Hit & Run TBI (O, Q). Scale bars: 25 μm.