ArticleJournal of neurochemistry2009
Real-time visualization of cytoplasmic calpain activation and calcium deregulation in acute glutamate excitotoxicity.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Mitochondrial Calcium Uniporter protects hippocampal CA2 neurons from NMDA-induced excitotoxic injury.Molecular medicine (Cambridge, Mass.) · 2026Article
- Article
- Calpain-Independent Intracellular Protease Activity Is Elevated in Excitotoxic Cortical Neurons Prior to Delayed Calcium Deregulation and Mitochondrial Dysfunction.Biomolecules · 2022Article
- Article
- Prevention of excitotoxicity-induced processing of BDNF receptor TrkB-FL leads to stroke neuroprotection.EMBO molecular medicine · 2019Article
- Insulin Protects Cortical Neurons Against Glutamate Excitotoxicity.Frontiers in neuroscience · 2019Article
- Inducible glutamate oxaloacetate transaminase as a therapeutic target against ischemic stroke.Antioxidants & redox signaling · 2015Review
- Ammonia mediates methamphetamine-induced increases in glutamate and excitotoxicity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Use of potentiometric fluorophores in the measurement of mitochondrial reactive oxygen species.Methods in enzymology · 2014Article
- Loss of OPA1 disturbs cellular calcium homeostasis and sensitizes for excitotoxicity.Cell death and differentiation · 2013Article
- Article
- Magnesium sulfate protects against the bioenergetic consequences of chronic glutamate receptor stimulation.PloS one · 2013Article
- Quantitative measurement of mitochondrial membrane potential in cultured cells: calcium-induced de- and hyperpolarization of neuronal mitochondria.The Journal of physiology · 2012Article
- Plasma membrane potential oscillations in insulin secreting Ins-1 832/13 cells do not require glycolysis and are not initiated by fluctuations in mitochondrial bioenergetics.The Journal of biological chemistry · 2012Article
- The role of glutamate in neuronal ischemic injury: the role of spark in fire.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Review
- Article
- Altered calcium signaling following traumatic brain injury.Frontiers in pharmacology · 2012Article
- Optogenetic reporters: Fluorescent protein-based genetically encoded indicators of signaling and metabolism in the brain.Progress in brain research · 2012Review
- Assessing mitochondrial dysfunction in cells.The Biochemical journal · 2011Review
- ChChd3, an inner mitochondrial membrane protein, is essential for maintaining crista integrity and mitochondrial function.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Although calpain (EC 3.4.22) protease activation was suggested to contribute to excitotoxic delayed calcium deregulation (DCD) via proteolysis of Na+/Ca2+ exchanger 3 (NCX3), cytoplasmic calpain activation in relation to DCD has never been visualized in real-time. We employed a calpain fluorescence resonance energy transfer substrate to simultaneously image calpain activation and calcium deregulation in live cortical neurons. A calpain inhibitor-sensitive decline in fluorescence resonance energy transfer was observed at 39 +/- 5 min after the occurrence of DCD in neurons exposed to continuous glutamate (100 microM). Inhibition of calpain by calpeptin did not delay the onset of DCD, recovery from DCD-like reversible calcium elevations, or cell death despite inhibiting alpha-spectrin processing by > 90%. NCXs reversed during glutamate exposure, the NCX antagonist KB-R7943 prolonged the time to DCD, and significant NCX3 cleavage following 90 min of glutamate exposure was not observed. Our findings suggest that robust calpain activation associated with acute glutamate toxicity occurs only after a sustained loss in calcium homeostasis. Processing of NCX3 or other calpain substrates is unlikely to be the primary cause of acute excitotoxicity in cortical neurons. However, a role for calpain as a contributing factor or in response to milder glutamate insults is not excluded.
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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.