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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Genetic inactivation of SARM1 axon degeneration pathway improves outcome trajectory after experimental traumatic brain injury based on pathological, radiological, and functional measures

Fig. 4

Sarm1 knockout reduces neuroinflammation at 10 weeks post-TBI. ad Representative images from CC coronal sections of Sarm1 WT (a, b) and Sarm1 KO (c, d) mice after sham (a, c) or TBI (b, d) procedures. Neuroinflammation is detected with markers of astrocytes (GFAP, green) and microglia (IBA1, red). DAPI nuclear stain shown in blue. The CC borders are indicated by dashed lines. eg Higher magnification examples of astrocyte (GFAP) and microglia (IBA1) morphology. In sham mice (e), astrocytes and microglia exhibit homeostatic morphology with thin processes. Following TBI (f, g), reactive astrocytes and microglia have intensely immunolabeled cell bodies and shorter, thicker, processes. h Sarm1 knockout significantly reduced astrogliosis after TBI, based on GFAP immunolabeling within the CC area. i The microglial response also indicated CC neuroinflammation after TBI, based on IBA1 immunolabeling, but did not detect differences due to Sarm1 inactivation. jk More detailed counting of IBA1 immunolabeled ( +) cells revealed that Sarm1 loss significantly reduced the frequency of both resting (j) and activated (k) microglia after TBI. Sarm1 WT: n = 7 sham, n = 7 TBI. Sarm1 KO: n = 6 sham, n = 7 TBI. ns = not significant. Further statistical details are provided in Additional File 1: Table S3. ad, scale bars = 100 µm. E–G, scale bars = 25 µm

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