ArticleInternational journal of molecular sciences2022
The Association between Hypoxia-Induced Low Activity and Apoptosis Strongly Resembles That between TTX-Induced Silencing and Apoptosis.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Metabolic Intervention with Dimethyl Malonate Impairs Phagocytic Clearance but Fails to Protect Neurons.bioRxiv : the preprint server for biology · 2026Article
- Phytochemical Diversity, Mechanistic Pharmacology, and Therapeutic Potential ofFoods (Basel, Switzerland) · 2026Review
- Protein Kinase C-β Inhibition and Survival Signaling after Simulated Cardioplegic-Ischemia/Reperfusion in Nondiabetic and Diabetic Human Coronary Arterial Endothelial Cells.Journal of the American College of Surgeons · 2025Article
- 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
- Oxygen gradient generator to improveFrontiers in neuroscience · 2023Article
- Cellular and Molecular Targets in Acute Ischemic Stroke.International journal of molecular sciences · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the penumbra of a brain infarct, neurons initially remain structurally intact, but perfusion is insufficient to maintain neuronal activity at physiological levels. Improving neuronal recovery in the penumbra has large potential to advance recovery of stroke patients, but penumbral pathology is incompletely understood, and treatments are scarce. We hypothesize that low activity in the penumbra is associated with apoptosis and thus contributes to irreversible neuronal damage. We explored the putative relationship between low neuronal activity and apoptosis in cultured neurons exposed to variable durations of hypoxia or TTX. We combined electrophysiology and live apoptosis staining in 42 cultures, and compared effects of hypoxia and TTX silencing in terms of network activity and apoptosis. Hypoxia rapidly reduced network activity, but cultures showed limited apoptosis during the first 12 h. After 24 h, widespread apoptosis had occurred. This was associated with full activity recovery observed upon reoxygenation within 12 h, but not after 24 h. Similarly, TTX exposure strongly reduced activity, with full recovery upon washout within 12 h, but not after 24 h. Mean temporal evolution of apoptosis in TTX-treated cultures was the same as in hypoxic cultures. These results suggest that prolonged low activity may be a common factor in the pathways towards apoptosis.
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Registered trials
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