Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency.

The reduction in rheobase and the shift in threshold potential induced by MPC1 deletion were accompanied by several changes in passive and active membrane properties governing cell excitability, including a significant increase in the input resistance (R i ) and in the voltage response to a depolarizing current injection (depol sub ), along with a marginally significant reduction in HCN channel-mediated sag ( Figure 5—figure supplement 1C-I ).

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