ArticleBiochemical and biophysical research communications2012
ATP activates P2X receptors to mediate gap junctional coupling in the cochlea.
Article in Biochemical and biophysical research communications, 2012. 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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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
24 citing papers in PubMed, 33 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
- Kolliker's Organ and Its Functional Role in the Development of Corti's Organ and Auditory Systems.Audiology research · 2025Review
- Differential Effects of Hearing Loss Mutations in Homomeric P2X2 and Heteromeric P2X2/3 Receptors.Cells · 2025Article
- Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.Biomedicines · 2022Review
- Purinergic Signalling in the Cochlea.International journal of molecular sciences · 2022Review
- Efferent neurons control hearing sensitivity and protect hearing from noise through the regulation of gap junctions between cochlear supporting cells.Journal of neurophysiology · 2022Article
- ATP and ACh Evoked Calcium Transients in the Neonatal Mouse Cochlear and Vestibular Sensory Epithelia.Frontiers in neuroscience · 2021Article
- Use of the guinea pig in studies on the development and prevention of acquired sensorineural hearing loss, with an emphasis on noise.The Journal of the Acoustical Society of America · 2019Review
- 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
- Spontaneous and Acetylcholine Evoked Calcium Transients in the Developing Mouse Utricle.Frontiers in cellular neuroscience · 2019Article
- Knockout of Pannexin-1 Induces Hearing Loss.International journal of molecular sciences · 2018Article
- P2X2 Dominant Deafness Mutations Have No Negative Effect on Wild-Type Isoform: Implications for Functional Rescue and in Deafness Mechanism.Frontiers in molecular neuroscience · 2017Article
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
- Adenosine Triphosphate (ATP) Inhibits Voltage-Sensitive Potassium Currents in Isolated Hensen's Cells and Nifedipine Protects Against Noise-Induced Hearing Loss in Guinea Pigs.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Expression and function of pannexins in the inner ear and hearing.BMC cell biology · 2016Review
- Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development.Scientific reports · 2015Article
- Cellular signaling protective against noise-induced hearing loss – A role for novel intrinsic cochlear signaling involving corticotropin-releasing factor?Biochemical pharmacology · 2015Review
- Pannexin1 channels dominate ATP release in the cochlea ensuring endocochlear potential and auditory receptor potential generation and hearing.Scientific reports · 2015Article
- Cellular and Deafness Mechanisms Underlying Connexin Mutation-Induced Hearing Loss - A Common Hereditary Deafness.Frontiers in cellular neuroscience · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
ATP is an important extracellular signaling molecule and can activate both ionotropic (P2X) and metabotropic purinergic (P2Y) receptors to influence cellular function in many aspects. Gap junction is an intercellular channel and plays a critical role in hearing. Here, we report that stimulation of ATP reduced gap junctional coupling between cochlear supporting cells. This uncoupling effect could be evoked by nanomolar physiological levels of ATP. A P2X receptor agonist benzoylbenzoyl-ATP (BzATP) but not a P2Y receptor agonist UTP stimulated this uncoupling effect. Application of P2X receptor antagonists pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 50μM) or oxidized ATP (oATP, 0.1mM) eliminated this uncoupling effect. We further found that ATP activated P2X receptors in the cochlear supporting cells allowing Ca(2+) influxing, thereby increasing intracellular Ca(2+) concentration to mediate gap junctions. These data suggest that ATP can mediate cochlear gap junctions at the physiological level by the activation of P2X receptors rather than P2Y receptors. This P2X receptor-mediated purinergic control on the cochlear gap junctions may play an important role in the regulation of K(+)-recycling for ionic homeostasis in the cochlea and the reduction of hearing sensitivity under noise stress for protection.
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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.