ArticleFrontiers in physiology2021
Paradoxical Potentiation of Acid-Sensing Ion Channel 3 (ASIC3) by Amiloride
Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Genetic deletion of ASIC3 alters left ventricular remodeling and autonomic function after myocardial infarction in mice.Physiological reports · 2026Article
- Genetic Deletion of ASIC3 Alters Left Ventricular Remodeling and Autonomic Function After Myocardial Infarction in Mice.bioRxiv : the preprint server for biology · 2025Article
- Epithelial NaComprehensive Physiology · 2024Review
- 4-(Azolyl)-Benzamidines as a Novel Chemotype for ASIC1a Inhibitors.International journal of molecular sciences · 2024Article
- Opioid Analgesic as a Positive Allosteric Modulator of Acid-Sensing Ion Channels.International journal of molecular sciences · 2024Article
- Physiological insight into the conserved properties of Caenorhabditis elegans acid-sensing degenerin/epithelial sodium channels.The Journal of physiology · 2023Article
- Drosophila ppk19 encodes a proton-gated and mechanosensitive ion channel.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Acid-Sensing Ion Channels (ASICs) are proton-gated sodium-selective cation channels that have emerged as metabolic and pain sensors in peripheral sensory neurons and contribute to neurotransmission in the CNS. These channels and their related degenerin/epithelial sodium channel (DEG/ENaC) family are often characterized by their sensitivity to amiloride inhibition. However, amiloride can also cause paradoxical potentiation of ASIC currents under certain conditions. Here we characterized and investigated the determinants of paradoxical potentiation by amiloride on ASIC3 channels. While inhibiting currents induced by acidic pH, amiloride potentiated sustained currents at neutral pH activation. These effects were accompanied by alterations in gating properties including (1) an alkaline shift of pH-dependent activation, (2) inhibition of pH-dependent steady-state desensitization (SSD), (3) prolongation of desensitization kinetics, and (4) speeding of recovery from desensitization. Interestingly, extracellular Ca
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