ArticleThe Journal of physiology2006
Extrusion of Ca2+ from mouse motor terminal mitochondria via a Na+-Ca2+ exchanger increases post-tetanic evoked release.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
- Post-ischemic inhibition of the mitochondrial Ca2+ uniporter with Ru265 protects in ex vivo and in vivo models of cerebral ischemia.Clinical science (London, England : 1979) · 2026Article
- Mitochondrial CaBiomolecules · 2026Review
- Monitoring presynaptic calcium dynamics with membrane-impermeant fluorescent indicators in motor nerve endings.Biophysical reviews · 2025Review
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Targeting paraptosis in cancer: opportunities and challenges.Cancer gene therapy · 2024Review
- Mitochondrial Mutations Can Alter Neuromuscular Transmission in Congenital Myasthenic Syndrome and Mitochondrial Disease.International journal of molecular sciences · 2023Review
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- A controversial issue: Can mitochondria modulate cytosolic calcium and contraction of skeletal muscle fibers?The Journal of general physiology · 2022Review
- Presynaptic Mitochondria Communicate With Release Sites for Spatio-Temporal Regulation of Exocytosis at the Motor Nerve Terminal.Frontiers in synaptic neuroscience · 2022Article
- Distinct properties of CaCell calcium · 2021Article
- Calcium is reduced in presynaptic mitochondria of motor nerve terminals during neurotransmission in SMA mice.Human molecular genetics · 2021Article
- Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions.Journal of visualized experiments : JoVE · 2018Article
- Ca2+ removal by the plasma membrane Ca2+-ATPase influences the contribution of mitochondria to activity-dependent Ca2+ dynamics in Aplysia neuroendocrine cells.Journal of neurophysiology · 2016Article
- Organelle-Specific Sensors for Monitoring CaFrontiers in synaptic neuroscience · 2016Review
- Stimulation-induced Ca(2+) influx at nodes of Ranvier in mouse peripheral motor axons.The Journal of physiology · 2016Article
- LRP4 is critical for neuromuscular junction maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Dysfunctional mitochondrial Ca(2+) handling in mutant SOD1 mouse models of fALS: integration of findings from motor neuron somata and motor terminals.Frontiers in cellular neuroscience · 2014Article
- Mitochondria and plasma membrane Ca2+-ATPase control presynaptic Ca2+ clearance in capsaicin-sensitive rat sensory neurons.The Journal of physiology · 2013Article
- Separate Ca2+ sources are buffered by distinct Ca2+ handling systems in aplysia neuroendocrine cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Motor terminal degeneration unaffected by activity changes in SOD1(G93A) mice; a possible role for glycolysis.Neurobiology of disease · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria sequester much of the Ca2+ that enters motor nerve terminals during repetitive stimulation at frequencies exceeding 10-20 Hz. We studied the post-stimulation extrusion of Ca2+ from mitochondria by measuring changes in matrix [Ca2+] with fluorescent indicators loaded into motor terminal mitochondria in the mouse levator auris longus muscle. Trains of action potentials at 50 Hz produced a rapid increase in mitochondrial [Ca2+] followed by a plateau, which was usually maintained after the end of the stimulus train and then slowly decayed back to baseline. Increasing the Ca2+ load delivered to the terminal by increasing the number of stimuli (from 500 to 2000) or the stimulation frequency (from 50 to 100 Hz), by increasing bath [Ca2+], or by prolonging the action potential with 3,4-diaminopyridine (100 microM) prolonged the post-stimulation decay of mitochondrial [Ca2+] without increasing the amplitude of the plateau during stimulation. Inhibiting the opening of the mitochondrial permeability transition pore with cyclosporin A (5 microM) had no significant effect on the decay of mitochondrial [Ca2+]. Inhibition of the mitochondrial Na+-Ca2+ exchanger with CGP-37157 (50 microM) dramatically prolonged the post-stimulation decay of mitochondrial [Ca2+], reduced post-stimulation residual cytosolic [Ca2+], and reduced the amplitude of endplate potentials evoked after the end of a stimulus train in the presence of both low and normal bath [Ca2+]. These findings suggest that Ca2+ extrusion from motor terminal mitochondria occurs primarily via the mitochondrial Na+-Ca2+ exchanger and helps to sustain post-tetanic transmitter release at mouse neuromuscular junctions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.