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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Neurobiol Aging. 2013 Nov 13;35(5):975–989. doi: 10.1016/j.neurobiolaging.2013.11.002

Figure 1. An Aβ1-42 oligomer-containing preparation induces an early increase in mitochondrial SO flash incidence in NPCs.

Figure 1

(A and B) Confocal images of mitochondrial SO in NPCs expressing mt-cpYFP that had been treated for 24 h with either vehicle control (A) or 0.5 μM Aβ1-42 OCP (B). Two supplemental videos showing mitochondrial SO flashes in NPCs that cover a 3 minute imaging period can be viewed online. The circled/numbered NPCs in panels A and B (cells n 1 and 2 cells in panel A and cells 1, 2, 3, 4 cells in B) exhibited a mitochondrial SO flash during the video recording period. Bar = 10 μm. (C and D) Sample recordings of mt-cpYFP fluorescence in NPCs that had been treated for 24 h with either vehicle control (C, cells 1 and 2 in panel A) or 0.5 μM Aβ1-42 OCP (D, cells 1 and 4 cells in panel B). Each arrow shows a SO flash. (E) SO flash incidence (percentage of cells with SO flash activity within 3 minutes of time-lapse imaging) plotted as percentage of control condition mean value (n = 3 separate experiments). *p<0.05 and **p<0.001compared to the control value. (F – H) The amplitude and kinetics of mitochondrial SO flashes in NPCs. ΔF/F0 is the amplitude of SO flashes where F0 refers to basal fluorescence intensity (F); Tp is the time to peak fluorescence intensity (G); and T50 is 50% decay time after the peak (H). *p<0.05 versus control (n=3 separate experiments, 80–120 flashes analyzed). (I) Global ROS level in NPCs measured using the probe DCF were not changed by treatment with 0.5, 1 μM or 5 μM Aβ1-42 OCP. (n = 3 separate experiments).