ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Mitochondrial ATP-Mg/Pi carrier SCaMC-3/Slc25a23 counteracts PARP-1-dependent fall in mitochondrial ATP caused by excitotoxic insults in neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 59 citations in OpenAlex.
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Calcium signaling in mitochondrial intermembrane space.Biochemical Society transactions · 2024Review
- Identification of potential biomarkers for aging diagnosis of mesenchymal stem cells derived from the aged donors.Stem cell research & therapy · 2024Article
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- Mitochondrial phosphoproteomes are functionally specialized across tissues.Life science alliance · 2024Article
- Variable bioenergetic sensitivity of neurons and astrocytes to insulin and extracellular glucose.npj metabolic health and disease · 2024Article
- Beyond the TCA cycle: new insights into mitochondrial calcium regulation of oxidative phosphorylation.Biochemical Society transactions · 2023Review
- How can childhood maltreatment affect post-traumatic stress disorder in adult: Results from a composite null hypothesis perspective of mediation analysis.Frontiers in psychiatry · 2023Article
- Two type I topoisomerases maintain DNA topology in human mitochondria.Nucleic acids research · 2022Article
- A CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Comprehensive Analysis and Validation of Solute Carrier Family 25 (SLC25) and Its Correlation with Immune Infiltration in Pan-Cancer.BioMed research international · 2022Article
- Embryonic periventricular endothelial cells demonstrate a unique pro-neurodevelopment and anti-inflammatory gene signature.Scientific reports · 2020Article
- Mitochondrial SLC25 Carriers: Novel Targets for Cancer Therapy.Molecules (Basel, Switzerland) · 2020Review
- Quantitative Imaging of Changes in Astrocytic and Neuronal Adenosine Triphosphate Using Two Different Variants of ATeam.Frontiers in cellular neuroscience · 2020Article
- Mortaparib, a novel dual inhibitor of mortalin and PARP1, is a potential drug candidate for ovarian and cervical cancers.Journal of experimental & clinical cancer research : CR · 2019Article
- The Response to Stimulation in Neurons and Astrocytes.Neurochemical research · 2019Review
- Insulin Protects Cortical Neurons Against Glutamate Excitotoxicity.Frontiers in neuroscience · 2019Article
- Mitochondrial CaPharmacology & therapeutics · 2018Review
- Calcium-regulated mitochondrial ATP-Mg/PIUBMB life · 2018Review
- Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases.Cell death and differentiation · 2018Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate excitotoxicity is caused by sustained activation of neuronal NMDA receptors causing a large Ca(2+) and Na(+) influx, activation of poly(ADP ribose) polymerase-1 (PARP-1), and delayed Ca(2+) deregulation. Mitochondria undergo early changes in membrane potential during excitotoxicity, but their precise role in these events is still controversial. Using primary cortical neurons derived from mice, we show that NMDA exposure results in a rapid fall in mitochondrial ATP in neurons deficient in SCaMC-3/Slc25a23, a Ca(2+)-regulated mitochondrial ATP-Mg/Pi carrier. This fall is associated with blunted increases in respiration and a delayed decrease in cytosolic ATP levels, which are prevented by PARP-1 inhibitors or by SCaMC-3 activity promoting adenine nucleotide uptake into mitochondria. SCaMC-3 KO neurons show an earlier delayed Ca(2+) deregulation, and SCaMC-3-deficient mitochondria incubated with ADP or ATP-Mg had reduced Ca(2+) retention capacity, suggesting a failure to maintain matrix adenine nucleotides as a cause for premature delayed Ca(2+) deregulation. SCaMC-3 KO neurons have higher vulnerability to in vitro excitotoxicity, and SCaMC-3 KO mice are more susceptible to kainate-induced seizures, showing that early PARP-1-dependent fall in mitochondrial ATP levels, counteracted by SCaMC-3, is an early step in the excitotoxic cascade.
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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.