ArticleFrontiers in cellular neuroscience2015
Acid-Sensing Ion Channels Expression, Identity and Role in the Excitability of the Cochlear Afferent Neurons.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Inhibition of delta-1 glutamate receptor current by extracellular protons.bioRxiv : the preprint server for biology · 2026Article
- Blocking acid-sensing ion channel 1a attenuates bilirubin-induced ototoxicity in cochlear organotypic culture.Fundamental research · 2026Article
- The Role of Zinc in Modulating Acid-Sensing Ion Channel Function.Biomolecules · 2023Review
- Diverse identities and sites of action of cochlear neurotransmitters.Hearing research · 2022Review
- Acid-Sensing Ion Channel 2: Function and Modulation.Membranes · 2022Review
- Acid-sensing ion channel 3: An analgesic target.Channels (Austin, Tex.) · 2021Review
- Acid-Sensing Ion Channels in Zebrafish.Animals : an open access journal from MDPI · 2021Review
- Locus Coeruleus Acid-Sensing Ion Channels Modulate Sleep-Wakefulness and State Transition from NREM to REM Sleep in the Rat.Neuroscience bulletin · 2021Article
- Cell-Type-Specific Expression Pattern of Proton-Sensing Receptors and Channels in Pituitary Gland.Biophysical journal · 2020Article
- Activating Acid-Sensing Ion Channels with Photoacid Generators.ChemPhotoChem · 2020Article
- Acid-sensing ion channels (ASICs) influence excitability of stellate neurons in the mouse cochlear nucleus.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2019Article
- Protons as Messengers of Intercellular Communication in the Nervous System.Frontiers in cellular neuroscience · 2018Review
- Glucose Deficiency Elevates Acid-Sensing Ion Channel 2a Expression and Increases Seizure Susceptibility in Temporal Lobe Epilepsy.Scientific reports · 2017Article
- Acid-Sensing Ion Channels as Potential Therapeutic Targets in Neurodegeneration and Neuroinflammation.Mediators of inflammation · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acid-sensing ion channels (ASICs) are activated by an increase in the extracellular proton concentration. There are four genes (ASIC1-4) that encode six subunits, and they are involved in diverse neuronal functions, such as mechanosensation, learning and memory, nociception, and modulation of retinal function. In this study, we characterize the ASIC currents of spiral ganglion neurons (SGNs). These ASIC currents are primarily carried by Na(+), exhibit fast activation and desensitization, display a pH50 of 6.2 and are blocked by amiloride, indicating that these are ASIC currents. The ASIC currents were further characterized using several pharmacological tools. Gadolinium and acetylsalicylic acid reduced these currents, and FMRFamide, zinc (at high concentrations) and N,N,N',N'-tetrakis-(2-piridilmetil)-ethylenediamine increased them, indicating that functional ASICs are composed of the subunits ASIC1, ASIC2, and ASIC3. Neomycin and streptomycin reduced the desensitization rate of the ASIC current in SGNs, indicating that ASICs may contribute to the ototoxic action of aminoglycosides. RT-PCR of the spiral ganglion revealed significant expression of all ASIC subunits. By immunohistochemistry the expression of the ASIC1a, ASIC2a, ASIC2b, and ASIC3 subunits was detected in SGNs. Although only a few SGNs exhibited action potential firing in response to an acidic stimulus, protons in the extracellular solution modulated SGN activity during sinusoidal stimulation. Our results show that protons modulate the excitability of SGNs via ASICs.
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