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. 2019 Sep 26;44(5):1801–1810. doi: 10.3892/ijmm.2019.4353

Figure 5.

Figure 5

HCN2 immunohistochemistry in the hippocampal CA1 region. HCN2 immunohistochemistry in the CA1 subfield of the (A) sham and (B-F) isch-emia-operated groups. HCN2 immunoreactivity is distinctly increased in CA1 pyramidal neurons 6 h after tgCI. Thereafter, HCN2 immunoreactivity is decreased with a time-dependent manner and very weakly observed in CA1 pyramidal neurons 4 days after tgCI. Scale bar, 50 µm. The asterisks and the arrows represent the CA1 pyramidal neurons and non-pyramidal cells, respectively. (G) ROD is presented as percentages of HCN2 immunoreactive structures in the CA1 subfield following tgCI (n=7 at each time point). *P<0.05 vs. the sham operated group. †P<0.05 vs. the previous timepoint group. Bars indicate the means ± standard error of the mean. (H-M) Double immunofluorescence staining for (H and K) HCN1 (green), (I) Kir6.1 (red), (L) GFAP (red) and (J and M) merged images in the stratum pyramidale 4 days after tgCI. HCN1 immunoreactivity was localized in Kir6.1-immunoreactive pericytes and GFAP-immunoreactive astrocytes. Arrows denote Kir6.1-immunoreactive pericytes and GFAP-immunoreactive astrocytes in the respective images. Scale bar, 20 µm. HCN2, hyperpolarization-activated cyclic nucleotide-gated 2; CA1, Cornu Ammonis 1; tgCI, transient global cerebral ischemia; ROD, relative optical density; Kir6.1, ATP-sensitive inward rectifier potassium channel 8; GFAP, anti-glial fibrillary acidic protein.