Skip to main content
. Author manuscript; available in PMC: 2017 Jan 12.
Published in final edited form as: Cell Metab. 2015 Nov 19;23(1):128–142. doi: 10.1016/j.cmet.2015.10.013

Figure 1. Neurons lacking SIRT3 exhibit increased vulnerability to excitotoxic, oxidative and metabolic stress.

Figure 1

(A) Representative merged phase-contrast and Hoechst dye fluorescence (blue) images of cultured cortical neurons from Sirt3+/+ and Sirt3−/− mice that had been exposed for 24 hours to the indicated agents. Viable neurons (indicated by yellow arrows) exhibit weak diffuse nuclear DNA-associated (Hoechst) fluorescence and intact neurites, whereas dying/dead neurons (indicated by red arrows) exhibit intense punctate Hoechst fluorescence as a result of nuclear chromatin condensation, and fragmented neurites. Treatment concentrations: 200 μM glutamate, 200 μM kainic acid (KA), 200 μM N-methyl-D-aspartate (NMDA). Scale bar = 20 μm. (B) Representative images of Hoechst staining (blue), and merged Tuj1 fluorescent immunostaining (green) and Hoechst staining of cultured neurons from Sirt3+/+ and Sirt3−/− mice that had been exposed to 200 μM glutamate for 24 h. Arrows indicate surviving Tuj1+ neurons and arrowheads indicate neurite fragmentation. (C–G) Results of quantitative analysis of neuronal death. Values are mean ± SEM of cell counts performed on cultures established from 4 or 5 mice. *p<0.05, **P<0.01.