Figure 7. Internalization of Ca_v1.3 channels reduced vulnerability of salamander RGCs to kainate-induced excitotoxicity.

Live/dead viability assay performed on retinal slices in normal Ringer solution (Control, A) exhibited healthy cells (coloured in green) throughout the retina. B, exposure of slices for 30 min to 100 μm kainate (Kain) promoted cell death in the ganglion cell layer (GCL) (arrowheads) and also few cells in the inner nuclear layer. C, prior incubation of slices for 30–40 min with 50 μm DIP (DIP/Kain) significantly enhanced kainate-induced cell death in the GCL. D, pre-incubation of slices with 10 μm cytochalasin D (CytD/Kain) markedly reduced kainate-induced RGC death. E, in contrast, stabilization of F-actin by 10 μm jasplakinolide (Jaspl/Kain) increased the number of kainate-induced dead cells (E). F, quantification summarizes these data indicating the role of endocytosis and cytoskeletal dynamics in excitotoxic RGC death. Each bar represents the number of dead cells per slice ±s.e.m. (n= 16–20 slices, *P < 0.05; **P < 0.01; 3 independent experiments). Statistical analysis was performed using ANOVA, followed by Tukey's post hoc test. Only cells in the GCL were considered for statistical analysis. Calibration bar, 50 μm.