ArticleThe Journal of physiology2003
Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 178 citations in OpenAlex.
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- Early Reduction in Mitochondrial Membrane Potential in Synaptic Mitochondria Contribute to Synaptic Pathology in the EAE Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Motor Neuron Size-Dependent Differences in mRNA Expression of Tropomyosin-Related Kinase Receptor B in Adult Rats.Journal of neurochemistry · 2026Article
- Mitochondrial CaBiomolecules · 2026Review
- MICU2 controls mitochondrial calcium signaling and migration in neurons during development.Cell reports · 2025Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Neurons and astrocytes have distinct organelle signatures and responses to stress.Cell reports · 2025Article
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Developmental changes of the mitochondria in the murine anteroventral cochlear nucleus.iScience · 2024Article
- Mitochondrial Mutations Can Alter Neuromuscular Transmission in Congenital Myasthenic Syndrome and Mitochondrial Disease.International journal of molecular sciences · 2023Review
- Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023Article
- Redox Imbalance as a Common Pathogenic Factor Linking Hearing Loss and Cognitive Decline.Antioxidants (Basel, Switzerland) · 2023Review
- Temperature- and chemical-induced neurotoxicity in zebrafish.Frontiers in physiology · 2023Review
- Neither too much nor too little: mitochondrial calcium concentration as a balance between physiological and pathological conditions.Frontiers in molecular biosciences · 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
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
44 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
We investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor terminals during brief trains of action potentials (500 at 50 Hz) in physiological bath [Ca2+]. When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulation-induced increase in cytosolic [Ca2+] was greater (> 10 microM, compared to < or = 1 microM in control solution), the quantal content of the endplate potential (EPP) depressed more rapidly (approximately 84 % depression compared to approximately 8 % in controls), and asynchronous release during the stimulus train reached higher frequencies (peak rates of approximately 6000 s-1 compared to approximately 75 s-1 in controls). These effects of mitochondrial depolarization were not accompanied by a significant change in EPP quantal content or the rate of asynchronous release during 1 Hz stimulation, and were not seen in oligomycin, which blocks mitochondrial ATP synthesis without depolarizing mitochondria. Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effect on stimulation-induced changes in cytosolic [Ca2+] or EPP amplitude. We hypothesize that the high rate of asynchronous release evoked by stimulation during mitochondrial depolarization was produced by the elevation of cytosolic [Ca2+], and contributed to the accelerated depression of phasic release by reducing the availability of releasable vesicles. During mitochondrial depolarization, the post-tetanic potentiation of the EPP observed under control conditions was replaced by a post-tetanic depression with a slow time course of recovery. Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release, and thus neuromuscular transmission, during and following tetanic stimulation.
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