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Increases in cytosolic Ca(2+) evoked by trains of action potentials (20-100 Hz) were recorded from mouse and lizard motor nerve terminals filled with a low-affinity fluorescent indicator, Oregon Green BAPTA 5N. In mouse terminals at near-physiological temperatures (30-38 degrees C), trains of action potentials at 25-100 Hz elicited increases in cytosolic Ca(2+) that stabilized at plateau levels that increased with stimulation frequency. Depolarization of mitochondria with carbonylcyanide m-chlorophenylhydrazone (CCCP) or antimycin A1 caused cytosolic Ca(2+) to rise to much higher levels during stimulation. Thus, mitochondrial Ca(2+) uptake contributes importantly to limiting the rise of cytosolic Ca(2+) during repetitive stimulation. In mouse terminals, the stimulation-induced increase in cytosolic Ca(2+) was highly temperature-dependent over the range 18-38 degrees C, with greater increases at lower temperatures. At the lower temperatures, application of CCCP continued to depolarize mitochondria but produced a much smaller increase in the cytosolic Ca(2+) transient evoked by repetitive stimulation. This result suggests that the larger amplitude of the stimulation-induced cytosolic Ca(2+) transient at lower temperatures was attributable in part to reduced mitochondrial Ca(2+) uptake. In contrast, the stimulation-induced increases in cytosolic Ca(2+) measured in lizard motor terminals showed little or no temperature-dependence over the range 18-33 degrees C.
David et al. (Sun,) studied this question.