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. Author manuscript; available in PMC: 2015 Aug 20.
Published in final edited form as: Neuron. 2014 Jul 31;83(4):975–988. doi: 10.1016/j.neuron.2014.07.001

FIGURE 7. Consequence of ATP deficit on the intracellular calcium concentration.

FIGURE 7

(A–C) Average [Ca++] after 2 s of tonic firing in the model driven by the synaptic inputs marked as red dots. The histograms show the relative contribution of each intra-cytosolic Ca++ regulation mechanism, with the Ca++ ATPases in red, the NCXs in green, and the MCU in blue.(A) Lowering the ATP availability mainly affects PMCA and SERCA, and leads to a large increase in the average [Ca++]. The ATPase deficit is not compensated by the intrinsic mitochondrial ATP-independent buffer mechanisms, the NCX exchanger or the MCU. (B) Although important, the MCU intrinsic mitochondrial buffer channel is not alone capable of compensating the loss of ATPase activity due to low ATP production, even for a smaller deficit than in A, with or without a modification of ΔΨ. (C) When mitochondria are removed entirely from a single dendrite (white arrow), the only buffering mechanism left is the NCX exchanger and it cannot preserve the Ca++ homeostasis in that region. Here histograms show Ca++ extrusion only in the affected compartment. (D) The dynamic range of the [Ca++] between the resting level and the peak level in some microdomain when an AP is fired for different [ATP]ss and ΔΨ, showing how mitochondria is essential for Ca++ homeostasis mainly through ATPase function and to a lesser extent, the NCX exchangers and the MCU.