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. Author manuscript; available in PMC: 2018 Jun 1.
Published in final edited form as: Neurobiol Dis. 2018 Mar 2;114:1–16. doi: 10.1016/j.nbd.2018.02.003

Fig. 7.

Fig. 7

Inhibition of axonal trafficking in neurons treated with soluble Aβ peptides does not affect mitochondrial function. (a) Parameters of mitochondrial respiration acquired in intact live primary neurons treated with different Aβ peptides using a Seahorse XF24 Extracellular Flux Analyzer. Measurements of oxygen consumption rates (OCR) in the absence or presence of specific mitochondrial toxins allows to estimate the following parameters: basal OCR (light blue); ATP-coupled respiration (dark blue) and proton leak (Uncoupled, yellow) after the addition of 1 μg/ml oligomycin; maximal (MRC, red) and spare (SRC, purple) respiratory capacity after an addition of 0.75 μM FCCP. The contribution of non-mitochondrial (green) respiration to basal OCR is determined as the activity remaining after the inhibition of complexes I and III with 0.75 μM rotenone and 0.75 μM antimycin A (AA). (b) Treatment of intact primary neurons with 2 μM Aβ42 (diamonds), 2 μM Aβ40H13G (circles) or 2 μM Aβ40 (triangles) did not affect mitochondrial energetics compared to neurons treated with vehicle (squares). Each data point is compiled from 6 to 8 individual wells from 3 independent experiments. (c) Analysis of the experiments conducted in (b). (d) Quantification of mitochondria coupling efficiency. (e) Estimation of mitochondria state apparent.