ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Na+-dependent sources of intra-axonal Ca2+ release in rat optic nerve during in vitro chemical ischemia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
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- Molecular machinery regulating mitochondrial calcium levels: The nuts and bolts of mitochondrial calcium dynamics.Mitochondrion · 2021Review
- IPNeurobiology of disease · 2020Article
- [Progress on axon regeneration in model organisms].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury.Frontiers in molecular neuroscience · 2020Article
- Regulation and dysregulation of axon infrastructure by myelinating glia.The Journal of cell biology · 2017Review
- The influence of sodium on pathophysiology of multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
- Sodium MRI of multiple sclerosis.NMR in biomedicine · 2016Review
- The Influence of Glutamate on Axonal Compound Action Potential In Vitro.Journal of brachial plexus and peripheral nerve injury · 2016Article
- Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation.Journal of neurophysiology · 2015Article
- Human macrophage SCN5A activates an innate immune signaling pathway for antiviral host defense.The Journal of biological chemistry · 2014Article
- Primary paranode demyelination modulates slowly developing axonal depolarization in a model of axonal injury.Journal of computational neuroscience · 2014Article
- The back and forth of axonal injury and repair after stroke.Current opinion in neurology · 2014Review
- Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon.Neurobiology of disease · 2013Review
- Inhibition of neuronal degenerin/epithelial Na+ channels by the multiple sclerosis drug 4-aminopyridine.The Journal of biological chemistry · 2013Article
- Axonal degeneration as a therapeutic target in the CNS.Cell and tissue research · 2012Review
- Axon degeneration: molecular mechanisms of a self-destruction pathway.The Journal of cell biology · 2012Review
- Wallerian degeneration: gaining perspective on inflammatory events after peripheral nerve injury.Journal of neuroinflammation · 2011Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of intracellular stores to axonal Ca2+ overload during chemical ischemia in vitro was examined by confocal microscopy. Ca2+ accumulation was measured by fluo-4 dextran (low-affinity dye, KD approximately 4 microM) or by Oregon Green 488 BAPTA-1 dextran (highaffinity dye, KD approximately 450 nM). Axonal Na+ was measured using CoroNa Green. Ischemia in CSF containing 2 mM Ca2+ caused an approximately 3.5-fold increase in fluo-4 emission after 30 min, indicating a large axonal Ca2+ rise well into the micromolar range. Axonal Na+ accumulation was enhanced by veratridine and reduced, but not abolished, by TTX. Ischemia in Ca2+-free (plus BAPTA) perfusate resulted in a smaller but consistent Ca2+ increase monitored by Oregon Green 488 BAPTA-1, indicating release from intracellular sources. This release was eliminated in large part when Na+ influx was reduced by replacement with N-methyl-D-glucamine (NMDG+; even in depolarizing high K+ perfusate), Li+, or by the application of TTX and significantly increased by veratridine. Intracellular release also was reduced significantly by neomycin or 1-(6-[(17beta-methoxyestra-1,3,5 [10]-trien-17-yl) amino] hexyl)-1H-pyrrole-2,5-dione (U73122 [GenBank]) (phospholipase C inhibitors), heparin [inositol trisphosphate (IP3) receptor blocker], or 7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one (CGP37157; mitochondrial Na+/Ca2+ exchange inhibitor) as well as ryanodine. Combining CGP37157 with U73122 [GenBank] or heparin decreased the response more than either agent alone and significantly improved electrophysiological recovery. Our conclusion is that intra-axonal Ca2+ release during ischemia in rat optic nerve is mainly dependent on Na+ influx. This Na+ accumulation stimulates three distinct intra-axonal sources of Ca2+: (1) the mitochondrial Na+/Ca2+ exchanger driven in the Na+ import/Ca2+ export mode, (2) positive modulation of ryanodine receptors, and (3) promotion of IP3 generation by phospholipase C.
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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.