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. 2009 Mar 13;33(5-3):627–638. doi: 10.1016/j.molcel.2009.02.013

Figure 1.

Figure 1

Characteristics of Mitochondrial Membrane Potential in PINK1 KD Neurons

(A) Immunofluorescence of human dopaminergic neurons (Ai) (blue, Hoechst; red, β3 tubulin; green, TH) and primary mouse neurons (Aii) (blue, Hoechst; red, GFAP; green, MAP). Scale bar, 10 μM.

(B) PINK1 KD neuroblastoma cells showed a 43% reduction (n > 120, p < 0.0001) in basal mitochondrial membrane potential (Δψm) compared to control cells (Bi). PINK1 KD human neurons exhibited 16% reduction (n > 60, p < 0.005) in basal Δψm compared to controls (Bii).

(C) In WT mouse neurons (Ci), oligomycin did not affect Δψm; rotenone induced partial depolarization; FCCP induced complete depolarization. In PINK1 KO mouse neurons (Cii), oligomycin induced mitochondrial depolarization (78.6% ± 4.8% decrease in Δψm, n = 72).

(D) Application of methyl succinate to PINK1 KO mouse neurons increased basal Δψm (19.5% ± 2.1%); application of pyruvate or malate to PINK1 KO neurons also increased the basal Δψm (18.6% ± 0.7%, n = 87). Substrate provision abolished oligomycin-induced mitochondrial depolarization in PINK1 KO.

Error bars represent mean ± SEM.