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. Author manuscript; available in PMC: 2015 May 25.
Published in final edited form as: Mol Cell Endocrinol. 2014 Feb 6;389(0):84–91. doi: 10.1016/j.mce.2013.12.019

Fig. 5. Antisense oligodeoxynucleotide (AS-ODN) knockdown of aromatase and brain-derived E2 levels in the hippocampal CA1 region of ovariectomized rats leads to enhanced neuronal damage and microglia activation following global cerebral ischemia (GCI).

Fig. 5

(A) Typical staining with NeuN of hippocampal sections from sham, GCI reperfusion 7 days (R7d), or GCI reperfusion 7 days aromatase AS-ODN or MS-ODN groups. (B) Quantitative analyses of the number of surviving neurons per 250μm length of medial CA1. NeuN-positive CA1 pyramidal cells showing intact and round nuclei were counted as surviving cells. Data are means±SE. *P<0.05 vs. sham, #P<0.05 vs. MS group. N = 5 per group. (C) Typical confocal microscopy images showing the double staining of iba1 and aromatase in hippocampal CA1 region from sham and GCI post reperfusion 7 days rats pretreated with aromatase AS-ODN or MS-ODN. Note that aromatase knockdown in ovariectomized rats leads to enhanced microglia activation, and that aromatase was not expressed in activated microglial cells. Scale bar, 50 μm. Magnification, 40×.