Stimulation-evoked increases in cytosolic [Ca(2+)] in mouse motor nerve terminals are limited by mitochondrial uptake and are temperature-dependent.

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.