TY - JOUR
T1 - Stimulation-evoked increases in cytosolic [Ca2+] in mouse motor nerve terminals are limited by mitochondrial uptake and are temperature-dependent
AU - David, G.
AU - Barrett, E. F.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2000/10/1
Y1 - 2000/10/1
N2 - Increases in cytosolic [Ca2+] evoked by trait 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 carbonylcyanide m-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.
AB - Increases in cytosolic [Ca2+] evoked by trait 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 carbonylcyanide m-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.
KW - Calcium indicator dyes
KW - Calcium sequestration
KW - Lizard
KW - Mitochondria
KW - Motor nerve terminal
KW - Neuromuscular junction
KW - Presynaptic terminal
KW - Temperature
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U2 - 10.1523/jneurosci.20-19-07290.2000
DO - 10.1523/jneurosci.20-19-07290.2000
M3 - Article
C2 - 11007886
AN - SCOPUS:0034307469
VL - 20
SP - 7290
EP - 7296
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 19
ER -