Fig. 2: Patient-derived DA neurons exhibited increased synaptic activity compared to control neurons. | npj Parkinson's Disease

Fig. 2: Patient-derived DA neurons exhibited increased synaptic activity compared to control neurons.

From: Upregulated ECM genes and increased synaptic activity in Parkinson’s human DA neurons with PINK1/ PRKN mutations

Fig. 2

Example recordings of EPSCs in (a) control DA neurons and (b) DA PINK1 and PRKN mutant neurons. c EPSC average amplitude was significantly larger in PINK1 and PRKN mutant neurons compared to control neurons. d DA PINK1 and PRKN mutant neurons showed significantly increased EPSC rates compared to control neurons. e The cumulative distribution of EPSC amplitudes was right shifted for PINK1 and PRKN mutant neurons, indicating higher EPSC amplitudes than for control neurons. f Dysregulated pathways in PINK1 and PRKN mutant DA neurons compared to healthy controls at 7–8 weeks post differentiation. Signaling network analysis with the top enriched KEGG pathways for the PINK1 and PRKN patient-derived neurons compared to the controls shows that the top dysregulated pathways for this double mutation are “ECM receptor interaction” and “Focal adhesion.” The red circle indicates a significantly up-regulated gene and the green indicates a significantly down-regulated gene (FDR < 0.05). 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.

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