ReviewJournal of neurochemistry2009
Contributions of Ca2+ and Zn2+ to spreading depression-like events and neuronal injury.
Review in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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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
23 citing papers in PubMed.
- Engineered bio-functional material-based nerve guide conduits for optic nerve regeneration: a view from the cellular perspective, challenges and the future outlook.Regenerative biomaterials · 2025Review
- Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice.Journal of visualized experiments : JoVE · 2024Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Synaptic ZnNeurobiology of disease · 2024Article
- Quantitative, real-time imaging of spreading depolarization-associated neuronal ROS production.Frontiers in cellular neuroscience · 2024Article
- Synaptic ZnbioRxiv : the preprint server for biology · 2023Article
- Is the Human Touch Always Therapeutic? Patient Stimulation and Spreading Depolarization after Acute Neurological Injuries.Translational stroke research · 2023Observational
- Migraine Aura, Transient Ischemic Attacks, Stroke, and Dying of the Brain Share the Same Key Pathophysiological Process in Neurons Driven by Gibbs-Donnan Forces, Namely Spreading Depolarization.Frontiers in cellular neuroscience · 2022Review
- Nimodipine Reappraised: An Old Drug With a Future.Current neuropharmacology · 2020Review
- Impact of mast cells in depression disorder: inhibitory effect of IL-37 (new frontiers).Immunologic research · 2018Review
- The continuum of spreading depolarizations in acute cortical lesion development: Examining Leão's legacy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Review
- Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Rose oil (from Rosa × damascena Mill.) vapor attenuates depression-induced oxidative toxicity in rat brain.Journal of natural medicines · 2013Article
- ZIP8 zinc transporter: indispensable role for both multiple-organ organogenesis and hematopoiesis in utero.PloS one · 2012Article
- Adaptation of microplate-based respirometry for hippocampal slices and analysis of respiratory capacity.Journal of neuroscience research · 2011Article
- Article
- Complex role of zinc in methamphetamine toxicity in vitro.Neuroscience · 2010Article
- Article
- Experimental and preliminary clinical evidence of an ischemic zone with prolonged negative DC shifts surrounded by a normally perfused tissue belt with persistent electrocorticographic depression.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The phenomenon of spreading depression (SD) involves waves of profound neuronal and glial depolarization that spread throughout brain tissue. Under many conditions, tissue recovers full function after SD has occurred, but SD-like events are also associated with spread of injury following ischemia or trauma. Initial large cytosolic Ca2+ increases accompany all forms of SD, but persistently elevated Ca2+ loading is likely responsible for neuronal injury following SD in tissues where metabolic capacity is insufficient to restore ionic gradients. Ca2+ channels are also involved in the propagation of SD, but the channel subtypes and cation fluxes differ significantly when SD is triggered by different types of stimuli. Ca2+ influx via P/Q type channels is important for SD generated by localized application of high K+ solutions. In contrast, SD-like events recorded in in vitro ischemia models are not usually prevented by Ca2+ removal, but under some conditions, Zn2+ influx via L-type channels contributes to SD initiation. This review addresses different roles of Ca2+ in the initiation and consequences of SD, and discusses recent evidence that selective chelation of Zn2+ can be sufficient to prevent SD under circumstances that may have relevance for ischemic injury.
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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.