ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Two distinct Ca(2+)-dependent signaling pathways regulate the motor output of cochlear outer hair cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 90 citations in OpenAlex.
- Perilymphatic ATP plays a critical role in modulating cochlear function to protect from loud sound induced hearing loss.EBioMedicine · 2026Article
- Modulation of BK-like potassium currents by ketamine in rat cochlear outer hair cells.Molecular brain · 2026Article
- Deep Learning-Based Prediction of Individual CellBiosensors · 2025Article
- Regulation of cochlear hair cell function by intracellular calcium stores.Frontiers in cellular neuroscience · 2024Article
- Synaptic Contributions to Cochlear Outer Hair Cell CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- SK Current, Expressed During the Development and Regeneration of Chick Hair Cells, Contributes to the Patterning of Spontaneous Action Potentials.Frontiers in cellular 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
- Oncomodulin: The Enigmatic Parvalbumin Protein.Frontiers in molecular neuroscience · 2019Article
- Oncomodulin, an EF-Hand Ca2+ Buffer, Is Critical for Maintaining Cochlear Function in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The Effects of Urethane on Rat Outer Hair Cells.Neural plasticity · 2016Article
- Deformation of the Outer Hair Cells and the Accumulation of Caveolin-2 in Connexin 26 Deficient Mice.PloS one · 2015Article
- Prestin at year 14: progress and prospect.Hearing research · 2014Review
- Functional regulation of the SLC26-family protein prestin by calcium/calmodulin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- ATP-gated ion channels mediate adaptation to elevated sound levels.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mammalian prestin is a weak Cl⁻/HCO₃⁻ electrogenic antiporter.The Journal of physiology · 2012Article
- Alterations of the CIB2 calcium- and integrin-binding protein cause Usher syndrome type 1J and nonsyndromic deafness DFNB48.Nature genetics · 2012Article
- The development, distribution and density of the plasma membrane calcium ATPase 2 calcium pump in rat cochlear hair cells.The European journal of neuroscience · 2012Article
- Calcium signaling in the cochlea - Molecular mechanisms and physiopathological implications.Cell communication and signaling : CCS · 2012Article
- Influence of acute hyperglycemia on otoacoustic emissions and the medial olivocochlear reflex.The Journal of the Acoustical Society of America · 2012Article
- Calcium-dependent inhibition of T-type calcium channels by TRPV1 activation in rat sensory neurons.Pflugers Archiv : European journal of physiology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The outer hair cells (OHCs) of the cochlea have an electromotility mechanism, based on conformational changes of voltage-sensitive "motor" proteins in the lateral plasma membrane. The translocation of electrical charges across the membrane that accompanies electromotility imparts a voltage dependency to the membrane capacitance. We used capacitance measurements to investigate whether electromotility may be influenced by different manipulations known to affect intracellular Ca(2+) or Ca(2+)-dependent protein phosphorylation. Application of acetylcholine (ACh) to the synaptic pole of isolated OHCs evoked a Ca(2+)-activated apamin-sensitive outward K(+) current. It also enhanced electromotility, probably because of a phosphorylation-dependent decrease of the cell's axial stiffness. However, ACh did not change the voltage-dependent capacitance either in conventional whole-cell experiments or under perforated-patch conditions. The effects produced by the Ca(2+) ionophore ionomycin mimicked those produced by ACh. Hyperpolarizing shifts of the voltage dependence of capacitance and electromotility were induced by okadaic acid, a promoter of protein phosphorylation, whereas trifluoperazine and W-7, antagonists of calmodulin, caused opposite depolarizing shifts. Components of the protein phosphorylation cascade-IP(3) receptors and calmodulin-dependent protein kinase type IV-were immunolocalized to the lateral wall of the OHC. Our results suggest that two different Ca(2+)-dependent pathways may control the OHC motor output. The first pathway modulates cytoskeletal stiffness and can be activated by ACh. The second pathway shifts the voltage sensitivity of the OHC electromotile mechanism and may be activated by the release of Ca(2+) from intracellular stores located in the proximity of the lateral plasma membrane.
Indexed as
Identifiers
10934241PMC6772567W2098924164What OpenQuestion holds
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.