ArticleThe Journal of general physiology2003
Mechanisms underlying modulation of neuronal KCNQ2/KCNQ3 potassium channels by extracellular protons.
Article in The Journal of general physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 64 citations in OpenAlex.
- Role of the C-terminal domain in modifying pH-dependent regulation of CaChannels (Austin, Tex.) · 2025Article
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- Carboxyl-group compounds activate voltage-gated potassium channels via a distinct mechanism.The Journal of general physiology · 2024Article
- Carbogen-Induced Respiratory Acidosis Blocks Experimental Seizures by a Direct and Specific Inhibition of NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Selective attenuation of Ether-a-go-go related KeLife · 2019Article
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- Modulation of Ether-à-Go-Go Related Gene (ERG) Current Governs Intrinsic Persistent Activity in Rodent Neocortical Pyramidal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Towards bridging the gap between acid-base transporters and neuronal excitability modulation.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Sub- and suprathreshold adaptation currents have opposite effects on frequency tuning.The Journal of physiology · 2012Article
- Kv1.1 knock-in ataxic mice exhibit spontaneous myokymic activity exacerbated by fatigue, ischemia and low temperature.Neurobiology of disease · 2012Article
- Distinct subunit contributions to the activation of M-type potassium channels by PI(4,5)P2.The Journal of general physiology · 2012Article
- Drosophila KCNQ channel displays evolutionarily conserved electrophysiology and pharmacology with mammalian KCNQ channels.PloS one · 2011Article
- Inhibition of K(Ca)2.2 and K(Ca)2.3 channel currents by protonation of outer pore histidine residues.The Journal of general physiology · 2009Article
- Article
- Extracellular pH modulates the voltage-dependent Ca2+ current and low threshold K+ current in hair cells.Neurochemical research · 2008Article
- Gonadotropin-releasing hormone (GnRH) activates the m-current in GnRH neurons: an autoregulatory negative feedback mechanism?Endocrinology · 2008Article
- The selectivity, voltage-dependence and acid sensitivity of the tandem pore potassium channel TASK-1: contributions of the pore domains.Pflugers Archiv : European journal of physiology · 2007Article
- Somatodendritic Kv7/KCNQ/M channels control interspike interval in hippocampal interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Experimental febrile seizures are precipitated by a hyperthermia-induced respiratory alkalosis.Nature medicine · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in extracellular pH occur during both physiological neuronal activity and pathological conditions such as epilepsy and stroke. Such pH changes are known to exert profound effects on neuronal activity and survival. Heteromeric KCNQ2/3 potassium channels constitute a potential target for modulation by H+ ions as they are expressed widely within the CNS and have been proposed to underlie the M-current, an important determinant of excitability in neuronal cells. Whole-cell and single-channel recordings demonstrated a modulation of heterologously expressed KCNQ2/3 channels by extracellular H+ ions. KCNQ2/3 current was inhibited by H+ ions with an IC50 of 52 nM (pH 7.3) at -60 mV, rising to 2 microM (pH 5.7) at -10 mV. Neuronal M-current exhibited a similar sensitivity. Extracellular H+ ions affected two distinct properties of KCNQ2/3 current: the maximum current attainable upon depolarization (Imax) and the voltage dependence of steady-state activation. Reduction of Imax was antagonized by extracellular K+ ions and affected by mutations within the outer-pore turret, indicating an outer-pore based process. This reduction of Imax was shown to be due primarily to a decrease in the maximum open-probability of single KCNQ2/3 channels. Single-channel open times were shortened by acidosis (pH 5.9), while closed times were increased. Acidosis also recruited a longer-lasting closed state, and caused a switch of single-channel activity from the full-conductance state ( approximately 8 pS) to a subconductance state ( approximately 5 pS). A depolarizing shift in the activation curve of macroscopic KCNQ2/3 currents and single KCNQ2/3 channels was caused by acidosis, while alkalosis caused a hyperpolarizing shift. Activation and deactivation kinetics were slowed by acidosis, indicating specific effects of H+ ions on elements involved in gating. Contrasting modulation of homomeric KCNQ2 and KCNQ3 currents revealed that high sensitivity to H+ ions was conferred by the KCNQ3 subunit.
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