Table 2.

Effect of BaCl₂ treatment on nuclear shrinkage after optic nerve crush.

Group	Nuclear Area (% of control) (Mean ± SD)	P1 value	P2 value
WT PBS	63.36 ± 19.27	1.44 × 10−68
WT BaCl2	75.19 ± 20.35	5.24 × 10−40	7.49 × 10−21
Bax−/− PBS	74.44 ± 22.17	1.36 × 10−54
Bax−/− BaCl2	95.22 ± 24.41	0.003	1.02 × 10−60

Cell shrinkage, often referred to the apoptotic volume decrease, is a common hallmark of programmed cell death. The shrinkage has been attributed to a rapid efflux of K⁺ ions through delayed rectifier potassium channels (Bortner and Cidlowski, 2007; Pal et al., 2003). We assessed if the shrinkage of nuclei in retinal ganglion cells was mediated by a similar K⁺ efflux, by blocking potassium channels with BaCl₂ (Bortner and Cidlowski, 2007). Left eyes of individual mice underwent optic nerve crush surgery and were then immediately injected with 1 µL of 1.5 mM BaCl₂ into the vitreous. Nuclear area (µm²) of cells in experimental retinas, 5 days after crush surgery, was calculated as a percentage of the mean area of nuclei in cells in control fellow retinas. PI values reflect comparisons of the nuclear areas of cells in control vs experimental eyes for each group (ANOVA). P2 values reflect comparison between the percent shrinkage of PBS vs BaCl₂-treated eyes for either wild type (WT) or Bax-deficient mice. At least 3 mice were evaluated in each group.