ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
A preferential role for glycolysis in preventing the anoxic depolarization of rat hippocampal area CA1 pyramidal cells.
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 49 papers.
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Who cites it
49 citing papers in PubMed, 99 citations in OpenAlex.
- ATP-depleting spreading depolarizations preferentially originate in the somatosensory cortex during in situ energy deprivation.npj metabolic health and disease · 2026Article
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- Serendipitous compound action potential oscillations reveal glycolytic astrocyte and oxidative axon interstitial KExperimental physiology · 2026Article
- Resveratrol Preconditioning Protects Against Ischemia-Induced Synaptic Dysfunction and Cofilin Hyperactivation in the Mouse Hippocampal Slice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Inhibition of high-voltage-activated calcium currents by acute hypoxia in cultured retinal ganglion cells.Frontiers in cellular neuroscience · 2023Article
- Energy matters: presynaptic metabolism and the maintenance of synaptic transmission.Nature reviews. Neuroscience · 2022Review
- Transforming a neural circuit to function without oxygen and glucose delivery.Current biology : CB · 2021Article
- Astrocyte Gliotransmission in the Regulation of Systemic Metabolism.Metabolites · 2021Review
- Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Flavin Adenine Dinucleotide Fluorescence as an Early Marker of Mitochondrial Impairment During Brain Hypoxia.International journal of molecular sciences · 2020Article
- Article
- Oxygen-Glucose Deprivation Differentially Affects Neocortical Pyramidal Neurons and Parvalbumin-Positive Interneurons.Neuroscience · 2019Article
- Fibre sub-type specific conduction reveals metabolic function in mouse sciatic nerve.The Journal of physiology · 2018Article
- Dissipation of transmembrane potassium gradient is the main cause of cerebral ischemia-induced depolarization in astrocytes and neurons.Experimental neurology · 2018Article
- Protein kinase C epsilon delays latency until anoxic depolarization through arc expression and GluR2 internalization.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Proton-gated Ca(2+)-permeable TRP channels damage myelin in conditions mimicking ischaemia.Nature · 2016Article
- A Prophylactic Role for Creatine in Hypoxia?The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Insulin neuroprotection and the mechanisms.Chinese medical journal · 2015Review
- Cancer as a mitochondrial metabolic disease.Frontiers in cell and developmental biology · 2015Article
- Reactive oxygen species initiate a metabolic collapse in hippocampal slices: potential trigger of cortical spreading depression.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
During brain anoxia or ischemia, a decrease in the level of ATP leads to a sudden decrease in transmembrane ion gradients [anoxic depolarization (AD)]. This releases glutamate by reversing the operation of glutamate transporters, which triggers neuronal death. By whole-cell clamping CA1 pyramidal cells, we investigated the energy stores that delay the occurrence of the AD in hippocampal slices when O2 and glucose are removed. With glycolytic and mitochondrial ATP production blocked in P12 slices, the AD occurred in approximately 7 min at 33 degrees C, reflecting the time needed for metabolic activity to consume the existing ATP and phosphocreatine, and for subsequent ion gradient decrease. Allowing glycolysis fueled by glycogen, in the absence of glucose, delayed the AD by 5.5 min, whereas superfused glucose prevented the AD for >1 h. With glycolysis blocked, the latency to the AD was 6.5 min longer when mitochondria were allowed to function, demonstrating that metabolites downstream of glycolysis (pyruvate, citric acid cycle intermediates, and amino acid oxidation) provide a significant energy store for oxidative phosphorylation. With glycolysis blocked but mitochondria functioning, superfusing lactate did not significantly delay the AD, showing that ATP production from lactate is much less than that from endogenous metabolites. These data demonstrate a preferential role for glycolysis in preventing the AD. They also define a hierarchy of pool sizes for hippocampal energy stores and suggest that brain ATP production from glial lactate may not be significant in conditions of energy deprivation.
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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.