ArticlePflugers Archiv : European journal of physiology2008
ATP activates P2x receptors and requires extracellular Ca(++) participation to modify outer hair cell nonlinear capacitance.
Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Perilymphatic ATP plays a critical role in modulating cochlear function to protect from loud sound induced hearing loss.EBioMedicine · 2026Article
- 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
- ATP-gated P2x7 receptors express at type II auditory nerves and required for efferent hearing control and noise protection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- 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 Modulation of Activity in the Developing Auditory Pathway.Neuroscience bulletin · 2020Review
- Hearing loss mutations alter the functional properties of human P2X2 receptor channels through distinct mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- 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
- 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
- Knockout of Pannexin-1 Induces Hearing Loss.International journal of molecular sciences · 2018Article
- Modulation of Glucose Takeup by Glucose Transport on the Isolated OHCs.Neural plasticity · 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
- Expression and function of pannexins in the inner ear and hearing.BMC cell biology · 2016Review
- Pannexin1 channels dominate ATP release in the cochlea ensuring endocochlear potential and auditory receptor potential generation and hearing.Scientific reports · 2015Article
- Connexin26 (GJB2) deficiency reduces active cochlear amplification leading to late-onset hearing loss.Neuroscience · 2015Article
- Cellular and Deafness Mechanisms Underlying Connexin Mutation-Induced Hearing Loss - A Common Hereditary Deafness.Frontiers in cellular neuroscience · 2015Review
- Non-synonymous single nucleotide polymorphisms in the P2X receptor genes: association with diseases, impact on receptor functions and potential use as diagnosis biomarkers.International journal of molecular sciences · 2014Review
- Aberrant Cx26 hemichannels and keratitis-ichthyosis-deafness syndrome: insights into syndromic hearing loss.Frontiers in cellular neuroscience · 2014Review
- The effects and outcomes of electrolyte disturbances and asphyxia on newborns hearing.International journal of pediatric otorhinolaryngology · 2013Article
- Mutation of the ATP-gated P2X(2) receptor leads to progressive hearing loss and increased susceptibility to noise.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Cell degeneration is not a primary causer for Connexin26 (GJB2) deficiency associated hearing loss.Neuroscience letters · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Intracochlear ATP is an important mediator in regulating hearing function. ATP can activate ionotropic purinergic (P2x) and metabotropic purinergic (P2y) receptors to influence cell functions. In this paper, we report that ATP can activate P2x receptors directly to modify outer hair cell (OHC) electromotility, which is an active cochlear amplifier determining hearing sensitivity and frequency selectivity in mammals. We found that ATP, but not UTP, a P2y receptor agonist, reduced the OHC electromotility-associated nonlinear capacitance (NLC) and shifted its voltage dependence to the right (depolarizing) direction. Blockage of the activation of P2x receptors by pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), suramin, and 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS) could block the ATP effect. This modification also required extracellular Ca(++) participation. Removal of extracellular Ca(++) abolished the ATP effect. However, chelation of intracellular Ca(++) concentration by a fast calcium-chelating reagent 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA, 10 mM) did not affect the effect of ATP on NLC. The effect is also independent of K(+) ions. Substitution of Cs(+) for intracellular or extracellular K(+) did not affect the ATP effect. Our findings indicate that ATP activates P2x receptors instead of P2y receptors to modify OHC electromotility. Extracellular Ca(++) is required for this modification.
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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.