ArticleThe Journal of biological chemistry2012
Impact of recovery from desensitization on acid-sensing ion channel-1a (ASIC1a) current and response to high frequency stimulation.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Conformational plasticity of human acid-sensing ion channel 1a.Nature structural & molecular biology · 2026Article
- Inhibition of delta-1 glutamate receptor current by extracellular protons.bioRxiv : the preprint server for biology · 2026Article
- Dynamic conformational changes of acid-sensing ion channels in different desensitizing conditions.Biophysical journal · 2024Article
- Modulation of Slow Desensitization (Tachyphylaxis) of Acid-Sensing Ion Channel (ASIC)1a.Cellular and molecular neurobiology · 2023Article
- Acid-sensing ion channels modulate bladder nociception.American journal of physiology. Renal physiology · 2021Article
- High-throughput characterization of photocrosslinker-bearing ion channel variants to map residues critical for function and pharmacology.PLoS biology · 2021Article
- β11-12 linker isomerization governs acid-sensing ion channel desensitization and recovery.eLife · 2020Article
- Slowing of the Time Course of Acidification Decreases the Acid-Sensing Ion Channel 1a Current Amplitude and Modulates Action Potential Firing in Neurons.Frontiers in cellular neuroscience · 2020Article
- Rapid resensitization of ASIC2a is conferred by three amino acid residues in the N terminus.The Journal of general physiology · 2019Article
- Acid-Sensing Ion Channels Activated by Evoked Released Protons Modulate Synaptic Transmission at the Mouse Calyx of Held Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- High-throughput electrophysiological assays for voltage gated ion channels using SyncroPatch 768PE.PloS one · 2017Article
- Functional and pharmacological characterization of two different ASIC1a/2a heteromers reveals their sensitivity to the spider toxin PcTx1.Scientific reports · 2016Article
- Acid-sensing ion channels are tuned to follow high-frequency stimuli.The Journal of physiology · 2016Article
- Regulating Factors in Acid-Sensing Ion Channel 1a Function.Neurochemical research · 2016Review
- Differential regulation of proton-sensitive ion channels by phospholipids: a comparative study between ASICs and TRPV1.PloS one · 2015Article
- Ion conduction and selectivity in acid-sensing ion channel 1.The Journal of general physiology · 2014Article
- A method for activation of endogenous acid-sensing ion channel 1a (ASIC1a) in the nervous system with high spatial and temporal precision.The Journal of biological chemistry · 2014Article
- Acid-sensing ion channels 1a (ASIC1a) inhibit neuromuscular transmission in female mice.American journal of physiology. Cell physiology · 2014Article
- Translational strategies for neuroprotection in ischemic stroke--focusing on acid-sensing ion channel 1a.Translational stroke research · 2014Review
- Protonation controls ASIC1a activity via coordinated movements in multiple domains.The Journal of general physiology · 2014Article
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3 authors.
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Abstract
backgroundConsecutive proton stimulation reduces ASIC1a peak currents leading to silencing of channels.
resultsKinetic analysis using a fast perfusion system shows that human ASIC1a has two desensitized states with markedly different stabilities.
conclusionHigh frequency trains of short stimuli prevent desensitization. SIGNIFICANCE: The results predict steady ASIC1a responses to high frequency release of protons as in synaptic transmission. ASIC1a is a neuronal sodium channel activated by external H(+) ions. To date, all the characterization of ASIC1a has been conducted applying long H(+) stimuli lasting several seconds. Such experimental protocols weaken and even silence ASIC1a currents to repetitive stimulation. In this work, we examined ASIC1a currents by methods that use rapid application and removal of H(+). We found that brief H(+) stimuli, <100 ms, even if applied at high frequency, prevent desensitization thereby generate full and steady peak currents of human ASIC1a. Kinetic analysis of recovery from desensitization of hASIC1a revealed two desensitized states: short- and long-lasting with time constants of τ(Ds) ≤0.5 and τ(Dl) = 229 s, while in chicken ASIC1a the two desensitized states have similar values τ(D) 4.5 s. It is the large difference in stability of the two desensitized states that makes hASIC1a desensitization more pronounced and complex than in cASIC1a. Furthermore, recovery from desensitization was unrelated to cytosolic variations in pH, ATP, PIP(2), or redox state but was dependent on the hydrophobicity of key residues in the first transmembrane segment (TM1). In conclusion, brief H(+)-stimuli maintain steady the magnitude of peak currents thereby the ASIC1a channel is well poised to partake in high frequency signals in the brain.
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