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. 2011 Mar 30;31(13):4962–4977. doi: 10.1523/JNEUROSCI.6417-10.2011

Figure 6.

Figure 6.

Death and opening of neuronal hemichannel induced by conditioned medium from Aβ25–35-treated glia is a hemichannel and NMDA/P2 receptor-dependent process. A, Et uptake ratio of neurons normalized to the effect of 3 h of incubation of CM harvested from Aβ25–35 (10 μm)-treated microglia (gray bars) or astrocytes (black bars) of Cx43−/− mice or CM made in the presence of Cx43E2, 10panx1 (200 μm), or Prob (200 μm). B, F-Jade labeling normalized to the effect of 3 h of incubation of CM harvested from Aβ25–35 (10 μm)-treated microglia (gray bars) or astrocytes (black bars) of Cx43−/− mice or CM made in the presence of Cx43E2, 10panx1 (200 μm), or Prob (200 μm). *p < 0.05, compared with 100% of CM effect. C, Averaged data normalized to the effect of 3 h of incubation of CM harvested from Aβ25–35 (10 μm)-treated microglia (gray bars) or astrocytes (black bars) on Et uptake ratio of neurons cotreated with 20 μm CPP (NMDA receptor blocker), 200 μm suramin (Sur) (P2 receptor blocker), 200 μm oATP (P2X receptor blocker), or 10 μm BBG (P2X7 receptor blocker) during CM incubation. D, Averaged data normalized to the effect of 3 h incubation with CM from microglia (gray bars) or astrocytes (black bars) on F-Jade labeling of neurons cotreated with 20 μm CPP and 200 μm suramin, 200 μm oATP, or 10 μm BBG during CM incubation. *p < 0.05, **p < 0.005, compared with 100% of CM effect. Averaged data are obtained from four independent experiments. Error bars indicate SEM.