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. 2017 Jan 1;34(1):248–256. doi: 10.1089/neu.2015.4355

FIG. 7.

FIG. 7.

Quantification of immunohistochemistry for SMI31 (A), myelin basic protein (MBP) (B), ionized calcium-binding adaptor molecule 1 (Iba1) (C), glial fibrillary acidic protein (GFAP) (D), and 4',6-diamidino-2-phenylindole (DAPI) (E) in the corpus callosum of normal (■) and ventriculomegaly (□) rats. SMI31 staining clearly demonstrates the loss of axonal staining at 1 day post-injury (DPI) and 8 DPI in the normal brain, whereas no significant changes in the axonal staining are seen in the ventriculomegaly brain (A). After injury, there is no significant loss of myelin by MBP staining in either group (B). Iba1 (C) and GFAP (D) show the increasing trend of microgliosis and astrogliosis, whereas excessively more Iba1 and GFAP-positive staining are shown in the ventriculomegaly brain. DAPI staining shows that both groups experience increased cellularity following mild traumatic brain injury, but the cellularity in the ventriculomegaly brain is significantly greater than that in the normal brain at 1 DPI. *p < 0.05, **p < 0.01.