Figure 4: Loss of synaptic input to patient iPSC-derived MNs. | Nature Communications

Figure 4: Loss of synaptic input to patient iPSC-derived MNs.

From: Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability

Figure 4

(a) Current responses in iPSC-derived MNs during bath application of glutamate (100 μM), GABA (100 μM) and glycine (100 μM). (b) Voltage-clamp recordings of spontaneous synaptic activity in iPSC-derived MNs at different holding potentials. (c) Proportion of cells displaying synaptic activity from weeks 3–10 post plating in iPSC-derived MNs from control (n=845), TARDBP (n=417) and C9ORF72 (n=265) lines. (*significantly different to control, P<0.05; ***significantly different to control, P<0.0001; logistic regression with multiple Wald’s tests and Bonferroni correction). (d) Graphs of inter-event interval and amplitude of synaptic events recorded from control and patient iPSC-derived MNs.

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