ArticleScientific reports2020
Reappraisal of anoxic spreading depolarization as a terminal event during oxygen-glucose deprivation in brain slices in vitro.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 22 citations in OpenAlex.
- Enhanced Response of ZnO Nanorod-Based Flexible MEAs for Recording Ischemia-Induced Neural Activity in Acute Brain Slices.Nanomaterials (Basel, Switzerland) · 2025Article
- Atypical plume-like events contribute to glutamate accumulation in metabolic stress conditions.iScience · 2025Article
- Pharmacological inhibition of all known major inward cationic currents does not block the induction of spreading depolarizations.Frontiers in cellular neuroscience · 2025Article
- Behavioral and Cognitive Consequences of Spreading Depolarizations: A Translational Scoping Review.Journal of neurotrauma · 2025Article
- Brief and Diverse Excitotoxic Insults Increase the Neuronal Nuclear Membrane Permeability in the Neonatal Brain, Resulting in Neuronal Dysfunction and Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Trauma in Neonatal Acute Brain Slices Alters Calcium and Network Dynamics and Causes Calpain-Mediated Cell Death.eNeuro · 2024Article
- Comparative Study of Terminal Cortical Potentials Using Iridium and Ag/AgCl Electrodes.International journal of molecular sciences · 2023Article
- Article
- Between life and death: the brain twilight zones.Frontiers in neuroscience · 2023Review
- Anoxic spreading depolarization in the neonatal rat cortexFrontiers in cellular neuroscience · 2023Article
- Depth-profile of impairments in endothelin-1 - induced focal cortical ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention.Neurocritical care · 2022Review
- Transient Hypoperfusion to Ischemic/Anoxic Spreading Depolarization is Related to Autoregulatory Failure in the Rat Cerebral Cortex.Neurocritical care · 2022Article
- Comparative analysis of spreading depolarizations in brain slices exposed to osmotic or metabolic stress.BMC neuroscience · 2021Article
- New Insights and Methods for Recording and Imaging Spontaneous Spreading Depolarizations and Seizure-Like Events in Mouse Hippocampal Slices.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anoxic spreading depolarization (aSD) has been hypothesized as a terminal event during oxygen-glucose deprivation (OGD) in submerged cortical slices in vitro. However, mechanical artifacts caused by aSD-triggered edema may introduce error in the assessment of neuronal viability. Here, using continuous patch-clamp recordings from submerged rat cortical slices, we first confirmed that vast majority of L4 neurons permanently lost their membrane potential during OGD-induced aSD. In some recordings, spontaneous transition from whole-cell to out-side out configuration occurred during or after aSD, and only a small fraction of neurons survived aSD with reperfusion started shortly after aSD. Secondly, to minimize artifacts caused by OGD-induced edema, cells were short-term patched following OGD episodes of various duration. Nearly half of L4 cells maintained membrane potential and showed the ability to spike-fire if reperfusion started less than 10 min after aSD. The probability of finding live neurons progressively decreased at longer reperfusion delays at a rate of about 2% per minute. We also found that neurons in L2/3 show nearly threefold higher resistance to OGD than neurons in L4. Our results suggest that in the OGD ischemia model, aSD is not a terminal event, and that the "commitment point" of irreversible damage occurs at variable delays, in the range of tens of minutes, after OGD-induced aSD in submerged cortical slices.
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