ArticlePloS one2016
Progression of Neuronal Damage in an In Vitro Model of the Ischemic Penumbra.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Trial
- 4-Chlorobenzylamine Containing Maleic Acid Derivatives: Synthesis,ACS chemical neuroscience · 2026Article
- Role of autophagy in neurotoxic protein's clearance following post-ischemic stroke: where we are and what we know?Molecular brain · 2025Review
- How to Pick a Neuroprotective Drug in Stroke Without Losing Your Mind?Life (Basel, Switzerland) · 2025Review
- Pathophysiologic Mechanisms of Severe Spinal Cord Injury and Neuroplasticity Following Decompressive Laminectomy and Expansive Duraplasty: A Systematic Review.Neurology international · 2025Review
- Cystatin C loaded in brain-derived extracellular vesicles rescues synapses after ischemic insult in vitro and in vivo.Cellular and molecular life sciences : CMLS · 2024Article
- Neuroprotective role of lactate in a human in vitro model of the ischemic penumbra.Scientific reports · 2024Article
- Hypothermia improves neuronal network recovery in a human-derived in vitro model of oxygen-deprivation.PloS one · 2024Article
- The Role of LincRNA-EPS/Sirt1/Autophagy Pathway in the Neuroprotection Process by Hydrogen against OGD/R-Induced Hippocampal HT22 Cells Injury.Journal of personalized medicine · 2023Article
- Article
- Oxygen gradient generator to improveFrontiers in neuroscience · 2023Article
- Nanomaterial-based microelectrode arrays for in vitro bidirectional brain-computer interfaces: a review.Microsystems & nanoengineering · 2023Review
- Promising Strategies for the Development of Advanced In Vitro Models with High Predictive Power in Ischaemic Stroke Research.International journal of molecular sciences · 2022Review
- The Association between Hypoxia-Induced Low Activity and Apoptosis Strongly Resembles That between TTX-Induced Silencing and Apoptosis.International journal of molecular sciences · 2022Article
- Neurovascular coupling and oxygenation are decreased in hippocampus compared to neocortex because of microvascular differences.Nature communications · 2021Article
- Dysregulation of Astrocyte Ion Homeostasis and Its Relevance for Stroke-Induced Brain Damage.International journal of molecular sciences · 2021Review
- Qingda granule exerts neuroprotective effects against ischemia/reperfusion-induced cerebral injury via lncRNA GAS5/miR-137 signaling pathway.International journal of medical sciences · 2021Article
- Ghrelin-Mediated Regeneration and Plasticity After Nervous System Injury.Frontiers in cell and developmental biology · 2021Review
- Translational Block in Stroke: A Constructive and "Out-of-the-Box" Reappraisal.Frontiers in neuroscience · 2021Article
- Neuroprotective mechanisms of DNA methyltransferase in a mouse hippocampal neuronal cell line after hypoxic preconditioning.Neural regeneration research · 2020Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Improvement of neuronal recovery in the ischemic penumbra around a brain infarct has a large potential to advance clinical recovery of patients with acute ischemic stroke. However, pathophysiological mechanisms leading to either recovery or secondary damage in the penumbra are not completely understood. We studied neuronal dynamics in a model system of the penumbra consisting of networks of cultured cortical neurons exposed to controlled levels and durations of hypoxia. Short periods of hypoxia (pO2≈20mmHg) reduced spontaneous activity, due to impeded synaptic function. After ≈6 hours, activity and connectivity partially recovered, even during continuing hypoxia. If the oxygen supply was restored within 12 hours, changes in network connectivity were completely reversible. For longer periods of hypoxia (12-30 h), activity levels initially increased, but eventually decreased and connectivity changes became partially irreversible. After ≈30 hours, all functional connections disappeared and no activity remained. Since this complete silence seemed unrelated to hypoxic depths, but always followed an extended period of low activity, we speculate that irreversible damage (at least partly) results from insufficient neuronal activation. This opens avenues for therapies to improve recovery by neuronal activation.
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