ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Exacerbated responses to oxidative stress by an Na(+) load in isolated nerve terminals: the role of ATP depletion and rise of [Ca(2+)](i).
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 73 citations in OpenAlex.
- Leber's hereditary optic neuropathy and multiple sclerosis: overlap between mitochondrial disease and neuroinflammation.Frontiers in neurology · 2025Review
- Sex differences in physiological response to increased neuronal excitability in a knockin mouse model of pediatric epilepsy.Clinical science (London, England : 1979) · 2024Article
- The protective effect ofPeerJ · 2021Article
- Roles Played by the NaNeurochemical research · 2020Article
- Quantitative Imaging of Changes in Astrocytic and Neuronal Adenosine Triphosphate Using Two Different Variants of ATeam.Frontiers in cellular neuroscience · 2020Article
- Comparative assessment of the effects of meso-2,3-dimercaptosuccinic acid and salinomycin on spleen function of cadmium-exposed mice.Environmental science and pollution research international · 2019Article
- Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.Journal of experimental neuroscience · 2016Review
- Oral Exposure to Atrazine Induces Oxidative Stress and Calcium Homeostasis Disruption in Spleen of Mice.Oxidative medicine and cellular longevity · 2016Article
- The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency.Mechanisms of ageing and development · 2011Review
- Neurons efficiently repair glutamate-induced oxidative DNA damage by a process involving CREB-mediated up-regulation of apurinic endonuclease 1.The Journal of biological chemistry · 2010Article
- Induction of oxidative stress and lipid peroxidation in rats chronically exposed to cypermethrin through dermal application.Journal of veterinary science · 2009Article
- Coupling diverse routes of calcium entry to mitochondrial dysfunction and glutamate excitotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Review: Mitochondria and disease progression in multiple sclerosis.Neuropathology and applied neurobiology · 2008Review
- Localized loss of Ca2+ homeostasis in neuronal dendrites is a downstream consequence of metabolic compromise during extended NMDA exposures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Review
- TRPMs and neuronal cell death.Pflugers Archiv : European journal of physiology · 2005Review
- Sodium influx pathways during and after anoxia in rat hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Generation of reactive oxygen species in the reaction catalyzed by alpha-ketoglutarate dehydrogenase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Initiation of neuronal damage by complex I deficiency and oxidative stress in Parkinson's disease.Neurochemical research · 2004Review
- Energetics and oxidative stress in synaptic plasticity and neurodegenerative disorders.Neuromolecular medicine · 2002Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have explored the consequences of a [Na(+)](i) load and oxidative stress in isolated nerve terminals. The Na(+) load was achieved by veratridine (5-40 microM), which allows Na(+) entry via a voltage-operated Na(+) channel, and oxidative stress was induced by hydrogen peroxide (0.1-0.5 mM). Remarkably, neither the [Na(+)](i) load nor exposure to H(2)O(2) had any major effect on [Ca(2+)](i), mitochondrial membrane potential (Deltapsim), or ATP level. However, the combination of an Na(+) load and oxidative stress caused ATP depletion, a collapse of Deltapsim, and a progressive deregulation of [Ca(2+)](i) and [Na(+)](i) homeostasis. The decrease in the ATP level was unrelated to an increase in [Ca(2+)](i) and paralleled the rise in [Na(+)](i). The loss of Deltapsim was prevented in the absence of Ca(2+) but unaltered in the presence of cyclosporin A. We conclude that the increased ATP consumption by the Na,K-ATPase that results from a modest [Na(+)](i) load places an additional demand on mitochondria metabolically compromised by an oxidative stress, which are unable to produce a sufficient amount of ATP to fuel the ATP-driven ion pumps. This results in a deregulation of [Na(+)](i) and [Ca(2+)](i), and as a result of the latter, collapse of Deltapsim. The vicious cycle generated in the combined presence of Na(+) load and oxidative stress could be an important factor in the neuronal injury produced by ischemia or excitotoxicity, in which the oxidative insult is superimposed on a disturbed Na(+) homeostasis.
Indexed as
Identifiers
10704483PMC6772497W1544086002What 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.