Acetazolamide Treatment Prevents Redistribution of Astrocyte Aquaporin 4 after Murine Traumatic Brain Injury
Acetazolamide treatment prevents TBI-induced AQP4 depolarization. Mice were subjected to sham surgery or closed-cortical impact surgery, and were treated 30 minutes after surgery with either DMSO vehicle (Veh) or acetazolamide (15 mg/kg, AZA). Mice were sacrificed at 3 days after injury. Immunohistochemical labeling for AQP4 (green), GFAP (red), and DAPI (blue) was performed, and representative confocal images are shown in (a) sham-DMSO-treated mice, (b) sham-acetazolamide (AZA) treated mice, (c) TBI-DMSO-treated mice, and (d) TBI-AZA treated mice. Inset images show areas of increased magnification. (e) Histogram plot of perivascular depolarization was measured as described in the methods section (n=6 mice/group; p<0.01 versus all other groups) (f) Histogram plot of GFAP immunolabeling expressed as a percentage of sham-DMSO-treated mice (n=6 mice/group; p<0.05 versus sham-DMSO or sham-AZA treated mice). Significance was measured using ANOVA followed by Tukeyâ€™s HSD test.
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