ArticleThe Journal of physiology2007
Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
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- Glycolysis selectively shapes the presynaptic action potential waveform.Journal of neurophysiology · 2016Article
- 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
- Mitochondrial membrane studies using impedance spectroscopy with parallel pH monitoring.PloS one · 2014Article
- OPA1 promotes pH flashes that spread between contiguous mitochondria without matrix protein exchange.The EMBO journal · 2013Article
- Canonical transient receptor potential 3 channels regulate mitochondrial calcium uptake.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mitochondrial free Ca²⁺ levels and their effects on energy metabolism in Drosophila motor nerve terminals.Biophysical journal · 2013Article
- Regulation of the mitochondrial proton gradient by cytosolic Ca²⁺ signals.Pflugers Archiv : European journal of physiology · 2012Review
- Quantitative measurement of mitochondrial membrane potential in cultured cells: calcium-induced de- and hyperpolarization of neuronal mitochondria.The Journal of physiology · 2012Article
- Perspectives on: SGP symposium on mitochondrial physiology and medicine: the renaissance of mitochondrial pH.The Journal of general physiology · 2012Review
- Cytosolic calcium coordinates mitochondrial energy metabolism with presynaptic activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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
- Dynamic regulation of the mitochondrial proton gradient during cytosolic calcium elevations.The Journal of biological chemistry · 2011Article
- Use of NAD(P)H and flavoprotein autofluorescence transients to probe neuron and astrocyte responses to synaptic activation.Neurochemistry international · 2010Review
- A novel role for fatty acid transport protein 1 in the regulation of tricarboxylic acid cycle and mitochondrial function in 3T3-L1 adipocytes.Journal of lipid research · 2009Article
- The Psi(m) depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To investigate mitochondrial responses to repetitive stimulation, we measured changes in NADH fluorescence and mitochondrial membrane potential (Psi(m)) produced by trains of action potentials (50 Hz for 10-50 s) delivered to motor nerve terminals innervating external intercostal muscles. Stimulation produced a rapid decrease in NADH fluorescence and partial depolarization of Psi(m). These changes were blocked when Ca2+ was removed from the bath or when N-type Ca2+ channels were inhibited with omega-conotoxin GVIA, but were not blocked when bath Ca2+ was replaced by Sr2+, or when vesicular release was inhibited with botulinum toxin A. When stimulation stopped, NADH fluorescence and Psi(m) returned to baseline values much faster than mitochondrial [Ca2+]. In contrast to findings in other tissues, there was usually little or no poststimulation overshoot of NADH fluorescence. These findings suggest that the major change in motor terminal mitochondrial function brought about by repetitive stimulation is a rapid acceleration of electron transport chain (ETC) activity due to the Psi(m) depolarization produced by mitochondrial Ca2+ (or Sr2+) influx. After partial inhibition of complex I of the ETC with amytal, stimulation produced greater Psi(m) depolarization and a greater elevation of cytosolic [Ca2+]. These results suggest that the ability to accelerate ETC activity is important for normal mitochondrial sequestration of stimulation-induced Ca2+ loads.
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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.