ArticlePurinergic signalling2010
ATP-mediated potassium recycling in the cochlear supporting cells.
Article in Purinergic signalling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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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Who cites it
39 citing papers in PubMed, 49 citations in OpenAlex.
- Upregulation of ATP-purinergic P2×2 receptors in the cochlea over-amplifies hearing sensitivity leading to hyperacusis and attenuation by antagonists.bioRxiv : the preprint server for biology · 2026Article
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- Connexins in Acquired Hearing Loss: Expanding Research Perspectives.Biomedicines · 2025Review
- Differential Effects of Hearing Loss Mutations in Homomeric P2X2 and Heteromeric P2X2/3 Receptors.Cells · 2025Article
- Bile Acid Application in Cell-Targeting for Molecular Receptors in Relation to Hearing: A Comprehensive Review.Current drug targets · 2024Review
- Purinergic Signalling in the Cochlea.International journal of molecular sciences · 2022Review
- Modelling inner ear development and disease using pluripotent stem cells - a pathway to new therapeutic strategies.Disease models & mechanisms · 2022Review
- Expression of KID syndromic mutation Cx26S17F produces hyperactive hemichannels in supporting cells of the organ of Corti.Frontiers in cell and developmental biology · 2022Article
- Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells.Journal of neurophysiology · 2022Article
- Purinergic Signaling Controls Spontaneous Activity in the Auditory System throughout Early Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Excess extracellular KCommunications biology · 2021Article
- Connexin30-Deficiency Causes Mild Hearing Loss With the Reduction of Endocochlear Potential and ATP Release.Frontiers in cellular neuroscience · 2021Article
- Charging Up the Periphery: Glial Ionic Regulation in Sensory Perception.Frontiers in cell and developmental biology · 2021Review
- Article
- Purinergic Signaling and Cochlear Injury-Targeting the Immune System?International journal of molecular sciences · 2019Review
- Efficient introduction of an isogenic homozygous mutation to induced pluripotent stem cells from a hereditary hearing loss family using CRISPR/Cas9 and single-stranded donor oligonucleotides.The Journal of international medical research · 2019Article
- Connexin hemichannels and cochlear function.Neuroscience letters · 2019Review
- Knockout of Pannexin-1 Induces Hearing Loss.International journal of molecular sciences · 2018Article
- A deafness mechanism of digenic Cx26 (GJB2) and Cx30 (GJB6) mutations: Reduction of endocochlear potential by impairment of heterogeneous gap junctional function in the cochlear lateral wall.Neurobiology of disease · 2017Article
- Amplification mode differs along the length of the mouse cochlea as revealed by connexin 26 deletion from specific gap junctions.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledGap junction-mediated K(+) recycling in the cochlear supporting cell has been proposed to play a critical role in hearing. However, how potassium ions enter into the supporting cells to recycle K(+) remains undetermined. In this paper, we report that ATP can mediate K(+) sinking to recycle K(+) in the cochlear supporting cells. We found that micromolar or submicromolar levels of ATP could evoke a K(+)-dependent inward current in the cochlear supporting cells. At negative membrane potentials and the resting membrane potential of -80 mV, the amplitude of the ATP-evoked inward current demonstrated a linear relationship to the extracellular concentration of K(+), increasing as the extracellular concentration of K(+) increased. The inward current also increased as the concentration of ATP was increased. In the absence of ATP, there was no evoked inward current for extracellular K(+) challenge in the cochlear supporting cells. The ATP-evoked inward current could be inhibited by ionotropic purinergic (P2X) receptor antagonists. Application of pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 50 microM) or pre-incubation with an irreversible P2X7 antagonist oxidized ATP (oATP, 0.1 mM) completely abolished the ATP-evoked inward current at the negative membrane potential. ATP also evoked an inward current at cell depolarization, which could be inhibited by intracellular Cs(+) and eliminated by positive holding potentials. Our data indicate that ATP can activate P2X receptors to recycle K(+) in the cochlear supporting cells at the resting membrane potential under normal physiological and pathological conditions. This ATP-mediated K(+) recycling may play an important role in the maintenance of cochlear ionic homeostasis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11302-010-9184-9) contains supplementary material, which is available to authorized users.
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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.