ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
ASIC1a-specific modulation of acid-sensing ion channels in mouse cortical neurons by redox reagents.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Modulation of acid-sensing ion channel activity by nitric oxide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Trial
- Acid-sensing ion channels in the vasculature: emerging roles in systemic and pulmonary circulations.Pflugers Archiv : European journal of physiology · 2026Review
- Acid-sensing ion channel 1a promotes alcohol-associated liver disease in mice via regulating endoplasmic reticulum autophagy.Acta pharmacologica Sinica · 2025Article
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- Inhibition of Acid-Sensing Ion Channels by KB-R7943, a Reverse NaBiomolecules · 2023Article
- Upregulation of acid sensing ion channel 1a (ASIC1a) by hydrogen peroxide through the JNK pathway.Acta pharmacologica Sinica · 2021Article
- Hydrogen Sulfide Upregulates Acid-sensing Ion ChannelsFunction (Oxford, England) · 2021Article
- Changes in HFrontiers in cellular neuroscience · 2021Article
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 2020Review
- Factors and Molecular Mechanisms Influencing the Protein Synthesis, Degradation and Membrane Trafficking of ASIC1a.Frontiers in cell and developmental biology · 2020Review
- Redox Regulation of Ion Channels and Receptors in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Human ASIC1a mediates stronger acid-induced responses as compared with mouse ASIC1a.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Extracellular redox sensitivity of Kv1.2 potassium channels.Scientific reports · 2017Article
- Effect of Redox-Modifying Agents on the Activity of Channelrhodopsin-2.CNS neuroscience & therapeutics · 2017Article
- Regulating Factors in Acid-Sensing Ion Channel 1a Function.Neurochemical research · 2016Review
- σ-1 Receptor Inhibition of ASIC1a Channels is Dependent on a Pertussis Toxin-Sensitive G-Protein and an AKAP150/Calcineurin Complex.Neurochemical research · 2015Article
- Extracellular Subunit Interactions Control Transitions between Functional States of Acid-sensing Ion Channel 1a.The Journal of biological chemistry · 2015Article
- Chronic hypoxia limits H2O2-induced inhibition of ASIC1-dependent store-operated calcium entry in pulmonary arterial smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Acid-sensing ion channel (ASIC)-1a, the major ASIC subunit with Ca2+ permeability, is highly expressed in the neurons of CNS. Activation of these channels with resultant intracellular Ca2+ accumulation plays a critical role in normal synaptic plasticity, learning/memory, and in acidosis-mediated glutamate receptor-independent neuronal injury. Here we demonstrate that the activities of ASICs in CNS neurons are tightly regulated by the redox state of the channels and that the modulation is ASIC1a subunit dependent. In cultured mouse cortical neurons, application of the reducing agents dramatically potentiated, whereas the oxidizing agents inhibited the ASIC currents. However, in neurons from the ASIC1 knock-out mice, neither oxidizing agents nor reducing reagents had any effect on the acid-activated current. In Chinese Hamster Ovary cells, redox-modifying agents only affected the current mediated by homomeric ASIC1a, but not homomeric ASIC1b, ASIC2a, or ASIC3. In current-clamp recordings and Ca(2+)-imaging experiments, the reducing agents increased but the oxidizing agents decreased acid-induced membrane depolarization and the intracellular Ca2+ accumulation. Site-directed mutagenesis studies identified involvement of cysteine 61 and lysine 133, located in the extracellular domain of the ASIC1a subunit, in the modulation of ASICs by oxidizing and reducing agents, respectively. Our results suggest that redox state of the ASIC1a subunit is an important factor in determining the overall physiological function and the pathological role of ASICs in the CNS.
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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.