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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Neurobiol Dis. 2012 Jul 2;48(3):429–438. doi: 10.1016/j.nbd.2012.06.019

Figure 3. Increased GFAP expression in UC cortex is reduced toward naïve levels by chronic GBP treatment.

Figure 3

A: Representative images of GFAP-IR close to the UC lesion (dashed white lines) in sections from saline-treated (Saline UC, n = 6 rats), GBP-treated (GBP UC, 100mg/kg 3x/d x 7d, n = 6) and naive control cortex (n = 2). Pial surface up and to the left. Sections processed together and imaged using the same parameters. Increased GFAP-IR along cuts in Saline-UC is partially decreased toward naïve control level in GBP UC section. Lower images: NeuN-IR in sections adjacent to those in upper GFAP row to show laminar position of GFAP-IR. Roman numerals: cortical laminae. Calibration: 200 μm for all images

B: Western immunoblots of GFAP protein expression from UC cortex in 2 saline-treated rats (Saline 1 and Saline 2) and 2 UC rats treated with GBP (GBP1 and GBP2; 100 mg/kg 3xd x 7d). Cl: contralateral homotypic cortex. GFAP expression is increased in UC vs. contralateral cortex, and decreased in blots from GBP-treated vs. saline-treated UC animals.

C: Optical density of GFAP immunoblots normalized to the expression of β actin. Graphs show a significant decrease in GFAP expression in UC cortex for 3 and 7d GBP- vs. saline-treated UC rats. GBP dose/d as in B. *P < 0.05 for both comparisons. Data are expressed as mean ± SEM. Numbers of rats in bars.