ArticleProceedings of the National Academy of Sciences of the United States of America2009
The Psi(m) depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Warm Cells, Hot Mitochondria: Achievements and Problems of Ultralocal Thermometry.International journal of molecular sciences · 2023Review
- Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023Article
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Review
- Calcium is reduced in presynaptic mitochondria of motor nerve terminals during neurotransmission in SMA mice.Human molecular genetics · 2021Article
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
- A VDAC1-Derived N-Terminal Peptide Inhibits Mutant SOD1-VDAC1 Interactions and Toxicity in the SOD1 Model of ALS.Frontiers in cellular neuroscience · 2019Article
- Excitatory Dendritic Mitochondrial Calcium Toxicity: Implications for Parkinson's and Other Neurodegenerative Diseases.Frontiers in neuroscience · 2018Review
- Mitochondrial calcium uptake underlies ROS generation during aminoglycoside-induced hair cell death.The Journal of clinical investigation · 2016Article
- Impaired Autophagy and Defective Mitochondrial Function: Converging Paths on the Road to Motor Neuron Degeneration.Frontiers in cellular neuroscience · 2016Review
- Activity-dependent degeneration of axotomized neuromuscular synapses in Wld S mice.Neuroscience · 2015Article
- ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium Triad.Frontiers in cellular neuroscience · 2015Review
- Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Frontiers in cellular neuroscience · 2015Article
- ER-mitochondrial calcium flow underlies vulnerability of mechanosensory hair cells to damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Elevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice.Frontiers in cellular 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
- Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.The Journal of physiology · 2013Article
- Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset.PloS one · 2013Article
- Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The electrical gradient across the mitochondrial inner membrane (Psi(m)) is established by electron transport chain (ETC) activity and permits mitochondrial Ca(2+) sequestration. Using rhodamine-123, we determined how repetitive nerve stimulation (100 Hz) affects Psi(m) in motor terminals innervating mouse levator auris muscles. Stimulation-induced Psi(m) depolarizations in wild-type (WT) terminals were small (<5 mV at 30 degrees C) and reversible. These depolarizations depended on Ca(2+) influx into motor terminals, as they were inhibited when P/Q-type Ca(2+) channels were blocked with omega-agatoxin. Stimulation-induced Psi(m) depolarization and elevation of cytosolic [Ca(2+)] both increased when complex I of the ETC was partially inhibited by low concentrations of rotenone (25-50 nmol/l). This finding is consistent with the hypothesis that acceleration of ETC proton extrusion normally limits the magnitude of Psi(m) depolarization during mitochondrial Ca(2+) uptake, thereby permitting continued Ca(2+) uptake. Compared with WT, stimulation-induced increases in rhodamine-123 fluorescence were approximately 5 times larger in motor terminals from presymptomatic mice expressing mutations of human superoxide dismutase I (SOD1) that cause familial amyotrophic lateral sclerosis (SOD1-G85R, which lacks dismutase activity; SOD1-G93A, which retains dismutase activity). Psi(m) depolarizations were not significantly altered by expression of WT human SOD1 or knockout of SOD1 or by inhibiting opening of the mitochondrial permeability transition pore with cyclosporin A. We suggest that an early functional consequence of the association of SOD1-G85R or SOD1-G93A with motoneuronal mitochondria is reduced capacity of the ETC to limit Ca(2+)-induced Psi(m) depolarization, and that this impairment contributes to disease progression in mutant SOD1 motor terminals.
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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.