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. 2011 Oct 17;195(2):263–276. doi: 10.1083/jcb.201108059

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© 2011 Chen et al.

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Figure 5. — Bcl-x_L stabilizes the mitochondrial membrane potential to conserve energy. (A) A simplified model of ion flux across the inner mitochondrial membrane. Ions may enter or leave the matrix through leakage channels at point a (e.g., the F₁F_O ATP synthase through which protons enter the mitochondrial matrix), and overall stability and membrane potential are maintained by active pumps at point b (e.g., the ETC). The double arrow represents the source of fluctuation in potential. (B) Numerical simulations of the additional ion flux that occurs as a result of fluctuations in membrane potential using the 1-µm membrane vesicle model in A. An external perturbation with a fixed amplitude between 0 and 10 pA (5-ms duration) was allowed to occur randomly with a mean interval of 1 s, and the total ion flux was integrated over 20-s periods. The graph plots the increase in total integrated flux that results from fluctuations of increasing amplitude. (C) Numerical simulations of changes in mitochondrial inner membrane potential produced by stochastic opening of a nonselective cation channel. No openings occur when probability of channel opening (Po) equals 0, and the membrane is maintained at a steady level (−180 mV; dashed lines). Indicated opening rates of the channel produce fluctuations in membrane potential accompanied by net hyperpolarization (more negative potentials). (D) Mean ± SD of membrane potentials for traces in C.