ArticleInternational journal of physiology, pathophysiology and pharmacology2012
Inhibition of human acid-sensing ion channel 1b by zinc.
Article in International journal of physiology, pathophysiology and pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Acid-sensing ion channels and their role in controlling pain in the post-operative stage.International journal of physiology, pathophysiology and pharmacology · 2026Review
- Importance of Zinc Homeostasis for Normal Cardiac Rhythm.Current cardiology reviews · 2025Review
- Physiological insight into the conserved properties of Caenorhabditis elegans acid-sensing degenerin/epithelial sodium channels.The Journal of physiology · 2023Article
- The diverse functions of the DEG/ENaC family: linking genetic and physiological insights.The Journal of physiology · 2023Article
- The Role of Zinc in Modulating Acid-Sensing Ion Channel Function.Biomolecules · 2023Review
- Histidine Residues Are Responsible for Bidirectional Effects of Zinc on Acid-Sensing Ion Channel 1a/3 Heteromeric Channels.Biomolecules · 2020Article
- Regulating Factors in Acid-Sensing Ion Channel 1a Function.Neurochemical research · 2016Review
- The direct modulatory activity of zinc toward ion channels.Integrative medicine research · 2015Review
- Knockdown of acid-sensing ion channel 1a (ASIC1a) suppresses disease phenotype in SCA1 mouse model.Cerebellum (London, England) · 2014Article
- Acid-sensing ion channels: trafficking and synaptic function.Molecular brain · 2013Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Acid-sensing ion channel 1b (ASIC1b) is expressed in peripheral sensory neurons and has been implicated in nociception. Understanding the modulation of ASIC1b will provide important insight into how ASIC1b contributes to pain sensation. In our previous study, we showed that zinc, an important modulator of pain sensation, reduces rat ASIC1b current. However, rat ASIC1b shows several important differences from its recently identified human homolog. Most noticeably, human ASIC1b (hASIC1b) has a sustained component, which may play a role in persistent pain. Therefore, we tested here the hypothesis that zinc modulates the current properties of hASIC1b. Bath application of zinc suppressed the peak amplitude of hASIC1b currents, with a half-maximum inhibitory concentration of 37 μM. However, zinc did not affect the sustained component of hASIC1b currents. The effect of zinc was independent of pH-dependent activation, steady-state desensitization, and extracellular Ca(2+), suggesting noncompetitive mechanisms. Further, we found that extracellular site(s) of the hASIC1b subunit is important for the effect of zinc. Mutating cysteine 196, but not cysteine 309, in the extracellular domain of the hASIC1b abolished the zinc inhibition. These results suggest that, through modulating cysteine196, zinc may have a modulatory role in acute pain.
Indexed as
Identifiers
22837807PMC3403561W1497900627What 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.