ArticleJournal of neuroscience methods2010
A novel method for inducing focal ischemia in vitro.
Article in Journal of neuroscience methods, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Modeling Central Nervous System Injury In Vitro: Current Status and Promising Future Strategies.Biomedicines · 2022Review
- A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies.Current neuropharmacology · 2022Review
- 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 absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.Frontiers in cellular neuroscience · 2022Article
- A review of experimental models of focal cerebral ischemia focusing on the middle cerebral artery occlusion model.F1000Research · 2021Review
- Anti-inflammatory Effects of Traditional Chinese Medicines on PreclinicalFrontiers in pharmacology · 2019Review
- Neuroprotective Effects of Bioactive Compounds and MAPK Pathway Modulation in "Ischemia"-Stressed PC12 Pheochromocytoma Cells.Brain sciences · 2018Review
- Three-Dimensional Models of the Human Brain Development and Diseases.Advanced healthcare materials · 2018Review
- Ischemic stroke: experimental models and reality.Acta neuropathologica · 2017Review
- Review
- Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury.Scientific reports · 2014Article
- A review of creatine supplementation in age-related diseases: more than a supplement for athletes.F1000Research · 2014Review
- High temperatures alter physiological properties of pyramidal cells and inhibitory interneurons in hippocampus.Frontiers in cellular neuroscience · 2012Article
- Preclinical stroke research--advantages and disadvantages of the most common rodent models of focal ischaemia.British journal of pharmacology · 2011Review
- Sexual dimorphism in ischemic stroke: lessons from the laboratory.Women's health (London, England) · 2011Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Current in vitro models of stroke involve applying oxygen-glucose deprived (OGD) media over an entire brain slice or plate of cultured neurons. Thus, these models fail to mimic the focal nature of stroke as observed clinically and with in vivo rodent models of stroke. Our aim was to develop a novel in vitro brain slice model of stroke that would mimic focal ischemia and thus allow for the investigation of events occurring in the penumbra. This was accomplished by focally applying OGD medium to a small portion of a brain slice while bathing the remainder of the slice with normal oxygenated media. This technique produced a focal infarct on the brain slice that increased as a function of time. Electrophysiological recordings made within the flow of the OGD solution ("core") revealed that neurons rapidly depolarized (anoxic depolarization; AD) in a manner similar to that observed in other stroke models. Edaravone, a known neuroprotectant, significantly delayed this onset of AD. Electrophysiological recordings made outside the flow of the OGD solution ("penumbra") revealed that neurons within this region progressively depolarized throughout the 75 min of OGD application. Edaravone attenuated this depolarization and doubled neuronal survival. Finally, synaptic transmission in the penumbra was abolished within 50 min of focal OGD application. These results suggest that this in vitro model mimics events that occur during focal ischemia in vivo and can be used to determine the efficacy of therapeutics that target neuronal survival in the core and/or penumbra.
Indexed as
Identifiers
What OpenQuestion holds
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.