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. Author manuscript; available in PMC: 2015 Sep 10.
Published in final edited form as: Neuroendocrinology. 2014 Sep 10;100(0):129–140. doi: 10.1159/000367849

Fig. 1.

Fig. 1

CD11b/c+ area is increased by GCs and reversed by minocycline following KA injury. (A) Experimental design: Male rats were given 1 week to acclimate after arriving at our animal facility. GC manipulations were performed three days prior to KA, and brains were analyzed three days later. Indomethacin was injected every 12 h starting 24 h before KA. Minocycline was injected every 24 h starting 30 min before KA. (B) Representative images of CD11b/c staining in the hippocampal CA3 region 72 h post-injury. Scale bars = 500 μm, 100 μm inset. (C) The total amount of CD11b/c+ area was significantly lower in low GC treated rats compared with high GC rats. Minocycline significantly reduced CD11b/c signal in sham rats and high GC rats, but not low GC rats. Significance levels * p < 0.05 and ** p < 0.01 established by 2-way ANOVA followed by Holm-Sidak post hoc test. Significant 2-way ANOVA main effect of GC treatment (p < 0.05) and drug treatment (p < 0.0001). Sham, vehicle n = 7; low GC, vehicle n = 12; high GC, vehicle n = 6; Sham, indomethacin n = 6; low GC, indomethacin n = 5; high GC, indomethacin n = 9; Sham, minocycline n = 7; low GC, minocycline n = 7; high GC, minocycline n = 6.