ArticleScientific reports2019
Low oxygen post conditioning prevents thalamic secondary neuronal loss caused by excitotoxicity after cortical stroke.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Unravelling the nexus of stroke and dementia: Deciphering the role of secondary neurodegeneration in orchestrating cognitive decline.Neuroprotection (Chichester, England) · 2025Review
- Single-cell analysis identifies Ifi27l2a as a gene regulator of microglial inflammation in the context of aging and stroke in mice.Nature communications · 2025Article
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- Molecular Mechanism of Tetramethylpyrazine Ameliorating Neuroexcitotoxicity through Activating the PKA/CREB Signaling Pathway.BioMed research international · 2022Article
- Venous stroke-a stroke subtype that should not be ignored.Frontiers in neurology · 2022Review
- Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice.Neural plasticity · 2022Article
- Neuroinflammation as a Key Driver of Secondary Neurodegeneration Following Stroke?International journal of molecular sciences · 2021Review
- GluN3-Containing NMDA Receptors in the Rat Nucleus Accumbens Core Contribute to Incubation of Cocaine Craving.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- More than motor impairment: A spatiotemporal analysis of cognitive impairment and associated neuropathological changes following cortical photothrombotic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Corticosterone Administration Alters White Matter Tract Structure and Reduces Gliosis in the Sub-Acute Phase of Experimental Stroke.International journal of molecular sciences · 2021Article
- Determining the effect of aging, recovery time, and post-stroke memantine treatment on delayed thalamic gliosis after cortical infarct.Scientific reports · 2021Article
- Exploring How Low Oxygen Post Conditioning Improves Stroke-Induced Cognitive Impairment: A Consideration of Amyloid-Beta Loading and Other Mechanisms.Frontiers in neurology · 2021Article
- Growth Hormone Treatment Promotes Remote Hippocampal Plasticity after Experimental Cortical Stroke.International journal of molecular sciences · 2020Article
- Genetically Encoded Tools for Research of Cell Signaling and Metabolism under Brain Hypoxia.Antioxidants (Basel, Switzerland) · 2020Review
- Growth Hormone Promotes Motor Function after Experimental Stroke and Enhances Recovery-Promoting Mechanisms within the Peri-Infarct Area.International journal of molecular sciences · 2020Article
- Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke.Frontiers in neurology · 2020Review
- Oxytocin Receptor Signaling in Vascular Function and Stroke.Frontiers in neuroscience · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the current study, we were interested in investigating whether Low oxygen post-conditioning (LOPC) was capable of limiting the severity of stroke-induced secondary neurodegeneration (SND). To investigate the effect of LOPC we exposed adult male C57/BL6 mice to photothrombotic occlusion (PTO) of the motor and somatosensory cortex. This is known to induce progressive neurodegeneration in the thalamus within two weeks of infarction. Two days after PTO induction mice were randomly assigned to one of four groups: (i) LOPC-15 day exposure group; (ii) a LOPC 15 day exposure followed by a 15 day exposure to normal atmosphere; (iii) normal atmosphere for 15 days and (iv) normal atmosphere for 30 days (n = 20/group). We observed that LOPC reduced the extent of neuronal loss, as indicated by assessment of both area of loss and NeuN
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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.