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Increases in cytosolic [Ca2+] 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°C), trains of action potentials at 25–100 Hz elicited increases in cytosolic [Ca2+] that stabilized at plateau levels that increased with stimulation frequency. Depolarization of mitochondria with carbonylcyanidem-chlorophenylhydrazone (CCCP) or antimycin A1 caused cytosolic [Ca2+] to rise to much higher levels during stimulation. Thus, mitochondrial Ca2+uptake contributes importantly to limiting the rise of cytosolic [Ca2+] during repetitive stimulation. In mouse terminals, the stimulation-induced increase in cytosolic [Ca2+] was highly temperature-dependent over the range 18–38°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 [Ca2+] transient evoked by repetitive stimulation. This result suggests that the larger amplitude of the stimulation-induced cytosolic [Ca2+] transient at lower temperatures was attributable in part to reduced mitochondrial Ca2+ uptake. In contrast, the stimulation-induced increases in cytosolic [Ca2+] measured in lizard motor terminals showed little or no temperature-dependence over the range 18–33°C.

the journal of neuroscience/the journal of neuroscience

Stimulation-Evoked Increases in Cytosolic [Ca<sup>2+</sup>] in Mouse Motor Nerve Terminals Are Limited by Mitochondrial Uptake and Are Temperature-Dependent

Stimulation-Evoked Increases in Cytosolic [Ca2+] in Mouse Motor Nerve Terminals Are Limited by Mitochondrial Uptake and Are Temperature-Dependent

Stimulation-Evoked Increases in Cytosolic [Ca²⁺] in Mouse Motor Nerve Terminals Are Limited by Mitochondrial Uptake and Are Temperature-Dependent