ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011
Spreading depression and related events are significant sources of neuronal Zn2+ release and accumulation.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Spreading depolarization in neurocritical care: a review of SD'S pathophysiological continuum and clinical translation.Frontiers in human neuroscience · 2026Review
- Reperfusion and cytoprotective agents are a mutually beneficial pair in ischaemic stroke therapy: an overview of pathophysiology, pharmacological targets and candidate drugs focusing on excitotoxicity and free radical.Stroke and vascular neurology · 2024Review
- Synaptic ZnNeurobiology of disease · 2024Article
- Synaptic ZnbioRxiv : the preprint server for biology · 2023Article
- Memantine Improves Recovery After Spreading Depolarization in Brain Slices and can be Considered for Future Clinical Trials.Neurocritical care · 2021Article
- The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.Biomedicines · 2021Review
- Nimodipine Reappraised: An Old Drug With a Future.Current neuropharmacology · 2020Review
- Review
- High-resolution in vivo optical imaging of stroke injury and repair.Brain research · 2015Review
- Intramitochondrial Zn2+ accumulation via the Ca2+ uniporter contributes to acute ischemic neurodegeneration.Neurobiology of disease · 2014Article
- Chaos and commotion in the wake of cortical spreading depression and spreading depolarizations.Nature reviews. Neuroscience · 2014Review
- Zinc transporter-1 concentrates at the postsynaptic density of hippocampal synapses.Molecular brain · 2014Article
- The interactive roles of zinc and calcium in mitochondrial dysfunction and neurodegeneration.Journal of neurochemistry · 2014Article
- Intracellular dialysis disrupts Zn2+ dynamics and enables selective detection of Zn2+ influx in brain slice preparations.Journal of neurochemistry · 2013Article
- Intracellular Zn2+ accumulation enhances suppression of synaptic activity following spreading depolarization.Journal of neurochemistry · 2013Article
- Article
- Cytosolic acidification and intracellular zinc release in hippocampal neurons.Journal of neurochemistry · 2012Article
- Synaptic release and extracellular actions of Zn2+ limit propagation of spreading depression and related events in vitro and in vivo.Journal of neurophysiology · 2012Article
- The neurophysiology and pathology of brain zinc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Review
- Upregulation of KCC2 activity by zinc-mediated neurotransmission via the mZnR/GPR39 receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Spreading depression (SD) involves coordinated depolarizations of neurons and glia that propagate through the brain tissue. Repetitive SD-like events are common following human ischemic strokes, and are believed to contribute to the enlargement of infarct volume. Accumulation of Zn(2+) is also implicated in ischemic neuronal injury. Synaptic glutamate release contributes to SD propagation, and because Zn(2+) is costored with glutamate in some synaptic vesicles, we examined whether Zn(2+) is released by SD and may therefore provide a significant source of Zn(2+) in the postischemic period. Spreading depression-like events were generated in acutely prepared murine hippocampal slices by deprivation of oxygen and glucose (OGD), and Zn(2+) release was detected extracellularly by a Zn(2+)-selective indicator FluoZin-3. Deprivation of oxygen and glucose-SD produced large FluoZin-3 increases that propagated with the event, and signals were abolished in tissues from ZnT3 knockout animals lacking synaptic Zn(2+). Synaptic Zn(2+) release was also maintained with repetitive SDs generated by microinjections of KCl under normoxic conditions. Intracellular Zn(2+) accumulation in CA1 neurons, assessed using microinjection of FluoZin-3, showed significant increases following SD that was attributed to synaptic Zn(2+) release. These results suggest that Zn(2+) is released during SDs and could provide a significant source of Zn(2+) that contributes to neurodegeneration in the postischemic period.
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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.