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. 2012 Feb 10;29(3):589–599. doi: 10.1089/neu.2011.2059

FIG. 3.

FIG. 3.

Fibronectin treatment decreased dorsal column crush (DCC)-induced increases in blood–spinal cord barrier (BSCB) permeability, and the immunoreactivity of glial fibrillary acidic protein (GFAP) and ED1. (A) Rats with DCC were injected with fibronectin (DCC+FN, n=4). BSCB permeability to sodium fluorescein (NaF) was assessed in the tissues including at the epicenter (1-cm length of spinal cord surrounding the epicenter of lesion), and at the areas (1-cm-long) both rostral and caudal to the lesion of the spinal cord at 2 and 9 days after DCC. BSCB permeability changes are presented as the mean±standard deviation of NaF uptake in the tissues (μg NaF/μg tissue). Representative immunolabeling of GFAP (A–C, Normal, DCC, and DCC+FN), and ED1 (E–G) in the area caudal to the lesion demonstrated upregulation of GFAP (C) and ED1 (F), compared to normal rats (A and E) at 3 days after DCC. The graphs illustrate a significant increase after DCC (*versus normal rats), but a decrease with fibronectin treatment (xversus vehicle-treated DCC rats) in GFAP (D) and ED1 (H) immunoreactivity both rostral and caudal to the lesion (n=3 each group; N, normal rats; DC, vehicle-treated DCC rats; DC+FN, fibronectin-treated DCC rats; scale bar=100 mm).