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. 2017 Jan 18;37(3):726–737. doi: 10.1523/JNEUROSCI.3270-16.2016

Figure 4.

Figure 4.

MT-III deletion substantially eliminates the Zn2+ contribution to acute OGD-induced injury in CA1 (but not CA3) pyramidal neurons. CA1 and CA3 neurons in slices from MT-III KO mice were loaded with Fura-FF and FluoZin-3 and subjected to OGD alone (black) or with either TPEN (40 μm) or MK-801+ nimodipine (MK/Nim, each at 10 μm) as indicated (blue). Traces (±SEM; aligned for the onset of Ca2+ deregulation) show mean Fura-FF ratio changes. A, In the absence of MT-III, the protective effects of TPEN persist in CA3 (left) but are eliminated in CA1 (right) (CA3: control: 10.2 ± 0.7 min, n = 8, TPEN: 13.6 ± 0.7 min, n = 8, p = 3.7 × 10−3; CA1: control: 11.6 ± 0.7 min, n = 9, TPEN: 12.0 ± 0.8 min, n = 7, p = 0.76). B, In the absence of MT-III, NMDA- and VGCC-mediated excitotoxicity contributes substantially to OGD-evoked Ca2+ deregulation in both CA3 and CA1 pyramidal neurons (CA3: control: 10.2 ± 0.7 min, n = 8, MK/Nim: 17.2 ± 1.2 min, n = 7, p = 5.2 × 10−4; CA1: control: 13.0 ± 0.7 min, n = 9, MK/Nim: 20.4 ± 0.7 min, n = 10, p = 3.1 × 10−7; the MK/Nim-induced delay in Ca2+ deregulation was not different between CA3 and CA1, p = 0.78, ANOVA linear contrast).