ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Mitochondrial clearance of cytosolic Ca(2+) in stimulated lizard motor nerve terminals proceeds without progressive elevation of mitochondrial matrix [Ca(2+)].
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
49 citing papers in PubMed, 104 citations in OpenAlex.
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- Mitochondrial CaBiomolecules · 2026Review
- Mechanisms of delayed ischemia/reperfusion evoked ROS generation in the hippocampal CA1 zone of adult mouse brain slices.Scientific reports · 2025Article
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Presynaptic Mitochondria Communicate With Release Sites for Spatio-Temporal Regulation of Exocytosis at the Motor Nerve Terminal.Frontiers in synaptic neuroscience · 2022Article
- Calcium is reduced in presynaptic mitochondria of motor nerve terminals during neurotransmission in SMA mice.Human molecular genetics · 2021Article
- In vivo brain imaging of mitochondrial CaBiochimica et biophysica acta. Molecular cell research · 2021Review
- Glycolysis selectively shapes the presynaptic action potential waveform.Journal of neurophysiology · 2016Article
- Mitochondrial Ca(2+) Processing by a Unit of Mitochondrial Ca(2+) Uniporter and Na(+)/Ca(2+) Exchanger Supports the Neuronal Ca(2+) Influx via Activated Glutamate Receptors.Neurochemical research · 2016Article
- Stimulation-induced Ca(2+) influx at nodes of Ranvier in mouse peripheral motor axons.The Journal of physiology · 2016Article
- Enhanced synaptic transmission at the squid giant synapse by artificial seawater based on physically modified saline.Frontiers in synaptic neuroscience · 2014Article
- Exploring the central modulation hypothesis: do ancient memory mechanisms underlie the pathophysiology of trigger points?Current pain and headache reports · 2013Review
- Mitochondria and plasma membrane Ca2+-ATPase control presynaptic Ca2+ clearance in capsaicin-sensitive rat sensory neurons.The Journal of physiology · 2013Article
- Mitochondrial Ca(2+) and neurodegeneration.Cell calcium · 2012Review
- Dynamics of matrix-free Ca2+ in cardiac mitochondria: two components of Ca2+ uptake and role of phosphate buffering.The Journal of general physiology · 2012Article
- Mitochondria in motor nerve terminals: function in health and in mutant superoxide dismutase 1 mouse models of familial ALS.Journal of bioenergetics and biomembranes · 2011Review
- Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice.Neurobiology of disease · 2011Article
- Activity-dependent regulation of mitochondrial motility by calcium and Na/K-ATPase at nodes of Ranvier of myelinated nerves.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Presynaptic mitochondria in functionally different motor neurons exhibit similar affinities for Ca2+ but exert little influence as Ca2+ buffers at nerve firing rates in situ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Mitochondrial calcium function and dysfunction in the central nervous system.Biochimica et biophysica acta · 2009Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
This study used fluorescent indicator dyes to measure changes in cytosolic and mitochondrial [Ca(2+)] produced by physiological stimulation of lizard motor nerve terminals. During repetitive action potential discharge at 10-50 Hz, the increase in average cytosolic [Ca(2+)] reached plateau at levels that increased with increasing stimulus frequency. This stabilization of cytosolic [Ca(2+)] was caused mainly by mitochondrial Ca(2+) uptake, because drugs that depolarize mitochondria greatly increased the stimulation-induced elevation of cytosolic [Ca(2+)], whereas blockers of other Ca(2+) clearance routes had little effect. Surprisingly, during this sustained Ca(2+) uptake the free [Ca(2+)] in the mitochondrial matrix never exceeded a plateau level of approximately 1 microM, regardless of stimulation frequency or pattern. When stimulation ceased, matrix [Ca(2+)] decreased over a slow ( approximately 10 min) time course consisting of an initial plateau followed by a return to baseline. These measurements demonstrate that sustained mitochondrial Ca(2+) uptake is not invariably accompanied by progressive elevation of matrix free [Ca(2+)]. Both the plateau of matrix free [Ca(2+)] during stimulation and its complex decay after stimulation could be accounted for by a model incorporating reversible formation of an insoluble Ca salt. This mechanism allows mitochondria to sequester large amounts of Ca(2+) while maintaining matrix free [Ca(2+)] at levels sufficient to activate Ca(2+)-dependent mitochondrial dehydrogenases, but below levels that activate the permeability transition pore.
Indexed as
Identifiers
10460256PMC6782502W2097147236What OpenQuestion holds
Registered trials
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.