Fig. 1: Patient-derived DA neurons exhibited increased potassium currents compared to control neurons.

A representative evoked action potential trace in (a) control DA neurons and (b) DA PINK1 and PRKN mutant neurons. c The total evoked potential was not significantly different between control and PINK1 and PRKN mutant neurons. A representative picture of the spike shape of (d) control and (e) PINK1 and PRKN mutant neurons. f The 5 ms AHP was not different in neurons derived from PD patients with PINK1 and PRKN mutations compared to control neurons. g The spike height was significantly smaller in neurons derived from PD patients with PINK1 and PRKN mutations compared to healthy controls. Other spike shape features, i.e., h spike threshold and i capacitance, were not significantly different between patient-derived DA neurons and control neurons. Representative recordings of sodium and potassium currents in (j) control neurons and (k) PINK1 and PRKN mutant neurons. l Sodium current, m fast potassium currents, and n slow potassium currents were significantly increased in patient-derived DA neurons using a one-way ANOVA analysis. o DA neurons were characterized in culture using immunohistochemistry; Tyrosine Hydroxylase (TH) (green) specifically marks DA neurons in the culture (Scale bar 50 µm), DAPI (blue) stains nuclei, and MAP2 (red) marks neurons. The percentage of TH-positive neurons out of the MAP2-positive neurons is shown in Supplementary Fig. 3a and was 90.5 ± 1.9 in controls and 90 ± 4.2% in PINK1 and PRKN mutant neurons. Unless otherwise noted, the error bars in this and the following figures indicate the standard error. Asterisks in this figure denote statistical significance as indicated by the following codes: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.