ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Augmentation of M-type (KCNQ) potassium channels as a novel strategy to reduce stroke-induced brain injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Neuroprotective Effects, Mechanisms of Action and Therapeutic Potential of the Kv7/KCNQ Channel Opener QO-83 in Ischemic Stroke.Translational stroke research · 2025Article
- M-current modulation of cortical slow oscillations: Network dynamics and computational modeling.PLoS computational biology · 2023Article
- Redox regulation of KeLife · 2023Article
- Behavioral and neuro-functional consequences of eliminating the KCNQ3 GABA binding site in mice.Frontiers in molecular neuroscience · 2023Article
- Beyond Retigabine: Design, Synthesis, and Pharmacological Characterization of a Potent and Chemically Stable Neuronal Kv7 Channel Activator with Anticonvulsant Activity.Journal of medicinal chemistry · 2022Article
- KCNQ2 and KCNQ5 form heteromeric channels independent of KCNQ3.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization.Brain : a journal of neurology · 2021Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- KCNQ3 is the principal target of retigabine in CA1 and subicular excitatory neurons.Journal of neurophysiology · 2021Article
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Functional responses of the hippocampus to hyperexcitability depend on directed, neuron-specific KCNQ2 KHippocampus · 2020Article
- Enhancing KCNQ Channel Activity Improves Neurobehavioral Recovery after Spinal Cord Injury.The Journal of pharmacology and experimental therapeutics · 2020Article
- Kv7 Channels in Lung Diseases.Frontiers in physiology · 2020Review
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
- Pharmacological Manipulation of KFrontiers in physiology · 2020Review
- Photothrombotic Stroke as a Model of Ischemic Stroke.Translational stroke research · 2018Review
- M-type KBritish journal of pharmacology · 2018Review
- Effect of Hypokalemia on Functional Outcome at 3 Months Post-Stroke Among First-Ever Acute Ischemic Stroke Patients.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cerebral ischemic stroke is a worldwide cause of mortality/morbidity and thus an important focus of research to decrease the severity of brain injury. Therapeutic options for acute stroke are still limited. In neurons throughout the brain, "M-type" K(+) currents, underlain by KCNQ subunits 2-5, play dominant roles in control over excitability, and are thus implicated in myriad neurological and psychiatric disorders. Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their effects on ischemic injury remain unknown. Here, we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models. Both photothrombosis and MCAo led to rapid, predictable, and consistently sized necrotic brain lesions, inflammatory responses, and behavioral deficits. Administration of three distinct M-channel openers at 0-6 h after ischemic injury significantly decreased brain infarct size and inflammation, and prevented neurological dysfunction, although they were more effective when administered 0-3 h poststroke. Thus, we show beneficial effects against stroke-induced brain injury and neuronal death through pharmacological regulation of ion channels that control neuronal excitability.
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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.