ArticleJournal of neurochemistry2009
Simultaneous single neuron recording of O2 consumption, [Ca2+]i and mitochondrial membrane potential in glutamate toxicity.
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 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
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- Single-cell RNA sequencing reveals anterograde trans-synaptic degeneration and exacerbated synaptic remodeling in myopia.Experimental & molecular medicine · 2025Article
- Baicalin protects neurons from oxidative stress and apoptosis induced by glutamate excitotoxicity in HT-22 cells.Journal of veterinary science · 2025Article
- Activation of CaBulletin of experimental biology and medicine · 2021Article
- Neuroprotective Effect of Tricyclic Pyridine Alkaloids fromAntioxidants (Basel, Switzerland) · 2020Article
- Brain Branched-Chain Amino Acids in Maple Syrup Urine Disease: Implications for Neurological Disorders.International journal of molecular sciences · 2020Review
- Mapping mitochondrial respiratory chain deficiencies by respirometry: Beyond the Mito Stress Test.Experimental neurology · 2020Article
- HIV-1 infection alters energy metabolism in the brain: Contributions to HIV-associated neurocognitive disorders.Progress in neurobiology · 2019Review
- Nicotine protects rat hypoglossal motoneurons from excitotoxic death via downregulation of connexin 36.Cell death & disease · 2017Article
- Single-cell time-lapse imaging of intracellular OCell death & disease · 2017Article
- Bioenergetics and redox adaptations of astrocytes to neuronal activity.Journal of neurochemistry · 2016Review
- L-Lactate-Mediated Neuroprotection against Glutamate-Induced Excitotoxicity Requires ARALAR/AGC1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Article
- The metabolic response to excitotoxicity - lessons from single-cell imaging.Journal of bioenergetics and biomembranes · 2015Review
- Mitochondrial ATP-Mg/Pi carrier SCaMC-3/Slc25a23 counteracts PARP-1-dependent fall in mitochondrial ATP caused by excitotoxic insults in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
- Magnesium sulfate protects against the bioenergetic consequences of chronic glutamate receptor stimulation.PloS one · 2013Article
- Brain lactate metabolism: the discoveries and the controversies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Review
- Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency.Brain research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In order to determine the sequence of cellular processes in glutamate toxicity, we simultaneously recorded O(2) consumption, cytosolic Ca(2+) concentration ([Ca(2+)](i)), and mitochondrial membrane potential (mDeltapsi) in single cortical neurons. Oxygen consumption was measured using an amperometric self-referencing platinum electrode adjacent to neurons in which [Ca(2+)](i) and mDeltapsi were monitored with Fluo-4 and TMRE(+), respectively, using a spinning disk laser confocal microscope. Excitotoxic doses of glutamate caused an elevation of [Ca(2+)](i) followed seconds afterwards by an increase in O(2) consumption which reached a maximum level within 1-5 min. A modest increase in mDeltapsi occurred during this time period, and then, shortly before maximal O(2) consumption was reached, the mDeltapsi, as indicated by TMRE(+) fluorescence, dissipated. Maximal O(2) consumption lasted up to 5 min and then declined together with mDeltapsi and ATP levels, while [Ca(2+)](i) further increased. mDeltapsi and [Ca(2+)](i) returned to baseline levels when neurons were treated with an NMDA receptor antagonist shortly after the [Ca(2+)](i) increased. Our unprecedented spatial and time resolution revealed that this sequence of events is identical in all neurons, albeit with considerable variability in magnitude and kinetics of changes in O(2) consumption, [Ca(2+)](i), and mDeltapsi. The data obtained using this new method are consistent with a model where Ca(2+) influx causes ATP depletion, despite maximal mitochondrial respiration, minutes after glutamate receptor activation.
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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.