ArticleThe European journal of neuroscience2009
Zn2+ regulates Kv2.1 voltage-dependent gating and localization following ischemia.
Article in The European journal of neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- A Kv2 inhibitor combination reveals native neuronal conductances consistent with Kv2/KvS heteromers.eLife · 2025Article
- Zinc, Copper, and Calcium: A Triangle in the Synapse for the Pathogenesis of Vascular-Type Senile Dementia.Biomolecules · 2024Review
- The AMIGO1 adhesion protein activates Kv2.1 voltage sensors.Biophysical journal · 2022Article
- The modulation of potassium channels by estrogens facilitates neuroprotection.Frontiers in cell and developmental biology · 2022Review
- Tyrosine Phosphorylation of the KInternational journal of molecular sciences · 2020Article
- The Redox Biology of Excitotoxic Processes: The NMDA Receptor, TOPA Quinone, and the Oxidative Liberation of Intracellular Zinc.Frontiers in neuroscience · 2020Review
- Excitotoxicity: Still Hammering the Ischemic Brain in 2020.Frontiers in neuroscience · 2020Review
- Article
- Two Distinct Secretory Pathways for Differential Kv2.1 Localization in Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Impact of Labile Zinc on Heart Function: From Physiology to Pathophysiology.International journal of molecular sciences · 2017Review
- Disruption of KNeuroscience · 2017Article
- Molecular Mechanism of Disease-Associated Mutations in the Pre-M1 Helix of NMDA Receptors and Potential Rescue Pharmacology.PLoS genetics · 2017Article
- GRIN2D Recurrent De Novo Dominant Mutation Causes a Severe Epileptic Encephalopathy Treatable with NMDA Receptor Channel Blockers.American journal of human genetics · 2016Article
- Zn(2+) -induced Ca(2+) release via ryanodine receptors triggers calcineurin-dependent redistribution of cortical neuronal Kv2.1 K(+) channels.The Journal of physiology · 2016Article
- Cyclin e1 regulates Kv2.1 channel phosphorylation and localization in neuronal ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Redistribution of Kv2.1 ion channels on spinal motoneurons following peripheral nerve injury.Brain research · 2014Article
- Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration.Translational stroke research · 2014Review
- Kv3 channel assembly, trafficking and activity are regulated by zinc through different binding sites.The Journal of physiology · 2013Article
- Zinc modulation of basal and β-adrenergically stimulated L-type Ca2+ current in rat ventricular cardiomyocytes: consequences in cardiac diseases.Pflugers Archiv : European journal of physiology · 2012Article
- Chronic zinc exposure decreases the surface expression of NR2A-containing NMDA receptors in cultured hippocampal neurons.PloS one · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The delayed-rectifier K(+) channel Kv2.1 exists in highly phosphorylated somatodendritic clusters. Ischemia induces rapid Kv2.1 dephosphorylation and a dispersal of these clusters, accompanied by a hyperpolarizing shift in their voltage-dependent activation kinetics. Transient modulation of Kv2.1 activity and localization following ischemia is dependent on a rise in intracellular Ca(2+)and the protein phosphatase calcineurin. Here, we show that neuronal free Zn(2+)also plays a critical role in the ischemic modulation of Kv2.1. We found that sub-lethal ischemia in cultured rat cortical neurons led to characteristic hyperpolarizing shifts in K(+) current voltage dependency and pronounced dephosphorylation of Kv2.1. Zn(2+)chelation, similar to calcineurin inhibition, attenuated ischemic induced changes in K(+) channel activation kinetics. Zn(2+)chelation during ischemia also blocked Kv2.1 declustering. Surprisingly, we found that the Zn(2+)rise following ischemia occurred in spite of calcineurin inhibition. Therefore, a calcineurin-independent rise in neuronal free Zn(2+) is critical in altering Kv2.1 channel activity and localization following ischemia. The identification of Zn(2+) in mediating ischemic modulation of Kv2.1 may lead to a better understanding of cellular adaptive responses to injury.
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Registered trials
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