ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Inhibition of the Ca²⁺-dependent K⁺ channel, KCNN4/KCa3.1, improves tissue protection and locomotor recovery after spinal cord injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
- Involvement of interaction between TRPM2 and IKCA1 in temperature-dependent movement and IL-1β production in mouse microglia.The journal of physiological sciences : JPS · 2026Article
- Niacin promotes motor function recovery after spinal cord injury via Hcar2-dependent microglia immunometabolic regulation.Clinical and translational medicine · 2026Article
- Cyclosporine A Accelerates Neurorecovery Transcriptional Trajectory in a Swine Model of Diffuse Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Non-conducting functions of potassium channels in cancer and neurological disease.Current topics in membranes · 2023Review
- Microglial ion channels: Key players in non-cell autonomous neurodegeneration.Neurobiology of disease · 2022Review
- Microglia at the Centre of Brain Research: Accomplishments and Challenges for the Future.Neurochemical research · 2022Review
- Ion Channel Dysfunction in Astrocytes in Neurodegenerative Diseases.Frontiers in physiology · 2022Review
- Microglial Potassium Channels: From Homeostasis to Neurodegeneration.Biomolecules · 2021Review
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
- Thermosensitive collagen/fibrinogen gels loaded with decorin suppress lesion site cavitation and promote functional recovery after spinal cord injury.Scientific reports · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Characterization of Convergent Suppression by UCL-2077 (3-(Triphenylmethylaminomethyl)pyridine), Known to Inhibit Slow Afterhyperpolarization, ofInternational journal of molecular sciences · 2020Article
- The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson's disease.Journal of neuroinflammation · 2019Article
- Microglial Drug Targets in AD: Opportunities and Challenges in Drug Discovery and Development.Frontiers in pharmacology · 2019Review
- Review
- CaJournal of neuroinflammation · 2018Article
- Involvement of TRPM4 in detrusor overactivity following spinal cord transection in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- CaBrain, behavior, and immunity · 2018Article
- Functional Roles of the Ca2+-activated K+ Channel, KCa3.1, in Brain Tumors.Current neuropharmacology · 2018Review
- Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Spinal cord injury (SCI) triggers inflammatory responses that involve neutrophils, macrophages/microglia and astrocytes and molecules that potentially cause secondary tissue damage and functional impairment. Here, we assessed the contribution of the calcium-dependent K⁺ channel KCNN4 (KCa3.1, IK1, SK4) to secondary damage after moderate contusion lesions in the lower thoracic spinal cord of adult mice. Changes in KCNN4 mRNA levels (RT-PCR), KCa3.1 protein expression (Western blots), and cellular expression (immunofluorescence) in the mouse spinal cord were monitored between 1 and 28 d after SCI. KCNN4 mRNA and KCa3.1 protein rapidly increased after SCI; double labeling identified astrocytes as the main cellular source accounting for this upregulation. Locomotor function after SCI, evaluated for 28 d in an open-field test using the Basso Mouse Scale, was improved in a dose-dependent manner by treating mice with a selective inhibitor of KCa3.1 channels, TRAM-34 (triarylmethane-34). Improved locomotor function was accompanied by reduced tissue loss at 28 d and increased neuron and axon sparing. The rescue of tissue by TRAM-34 treatment was preceded by reduced expression of the proinflammatory mediators, tumor necrosis factor-α and interleukin-1β in spinal cord tissue at 12 h after injury, and reduced expression of inducible nitric oxide synthase at 7 d after SCI. In astrocytes in vitro, TRAM-34 inhibited Ca²⁺ signaling in response to metabotropic purinergic receptor stimulation. These results suggest that blocking the KCa3.1 channel could be a potential therapeutic approach for treating secondary damage after spinal cord 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.