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. 2018 Nov 30;8:17522. doi: 10.1038/s41598-018-35725-5

Figure 6.

Figure 6

NMDA-induced DNA damage, lipid peroxidation, and cell death require both Ca2+ influx and ligand binding. (a) Double stranded DNA breaks are visualized by foci of γH2Ax immunoreactivity (red) after incubation with either NMDA or NMDA + 7CK + ionomycin, but not after incubation with NMDA + AP5 + ionomycin. Scale bar = 5 µm. (b) Quantification of results shown in a. (c) Increased lipid peroxidation after incubation with NMDA or NMDA + 7CK + ionomycin, but not after incubation with NMDA + AP5 + ionomycin. (d) Increased cell death after incubation with NMDA or NMDA + 7CK + ionomycin, but not after incubation with NMDA + AP5 + ionomycin or with ionomycin in the absence of NMDA. (e) Increased cell death after incubation with NMDA or NMDA + 7CK + voltage-gated calcium channel activation (Bay K8644 in 50 mM KCl and 5 mM CaCl2), but not after activation of voltage-gated calcium channels in the absence of NMDA. Treatment conditions are as in Figs 3 and 5. Data are means + s.e.m., expressed as fold increase over control. Cell death in the control groups was 21 ± 8%. n = 3–5; *p < 0.05 vs control.