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. 2014 Aug 6;34(32):10582–10591. doi: 10.1523/JNEUROSCI.1912-14.2014

Figure 8.

Figure 8.

GJs formed by Cx45 mediate bystander cell death under ischemic conditions. A, LY retrogradely labeled RGC somas and their axons in control retina of Het mouse, ischemic Het retina (B), Cx36−/− retina (C), and Cx45−/− retina (D). E, Immunoreactivity of GFAP in vertical sections of control retina and ischemic retinas of Het (F), Cx36−/− (G), and Cx45−/− (H) mice. After ischemia-reperfusion, the GFAP immunoreactivity was upregulated throughout the retinal layers of Het and Cx36−/−, but not Cx45−/− mice. I, Histogram represents the nuclear cell count (per 500 μm length of vertical sections) in the GCL of control (n = 54/n = 5), and ischemic retinas of Het (n = 28/n = 3), Cx36−/− (n = 24/n = 4), and Cx45−/− (n = 74/n = 5) mice. J, Quantification of GFAP immunofluorescence intensity in the ischemic retinas of Het (n = 24/n = 4), Cx36−/− (n = 24/n = 4), and Cx45−/− (n = 22/n = 4, p > 0.1) mice. **p < 0.001 versus control. Scale bars: A–D, 100 μm; E–H, 50 μm.