ArticlePloS one2014
Functional expression of Rat Nav1.6 voltage-gated sodium channels in HEK293 cells: modulation by the auxiliary β1 subunit.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- High-throughput multiplex voltage-clamp/current-clamp evaluation of acutely isolated neurons.Nature protocols · 2026Review
- Inhibition of sodium conductance by cannabigerol contributes to a reduction of dorsal root ganglion neuron excitability.British journal of pharmacology · 2022Article
- NaNaunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Functional reconstitution of rat NaNeurotoxicology · 2017Review
- Glycolysis selectively shapes the presynaptic action potential waveform.Journal of neurophysiology · 2016Article
- Low Somatic Sodium Conductance Enhances Action Potential Precision in Time-Coding Auditory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Effects of the β1 auxiliary subunit on modification of Rat Na(v)1.6 sodium channels expressed in HEK293 cells by the pyrethroid insecticides tefluthrin and deltamethrin.Toxicology and applied pharmacology · 2016Article
- Α- and β-subunit composition of voltage-gated sodium channels investigated with μ-conotoxins and the recently discovered μO§-conotoxin GVIIJ.Journal of neurophysiology · 2015Article
- Article
- Non-selective cation channels mediate chloroquine-induced relaxation in precontracted mouse airway smooth muscle.PloS one · 2014Article
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2 authors.
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Abstract
The Nav1.6 voltage-gated sodium channel α subunit isoform is abundantly expressed in the adult rat brain. To assess the functional modulation of Nav1.6 channels by the auxiliary β1 subunit we expressed the rat Nav1.6 sodium channel α subunit by stable transformation in HEK293 cells either alone or in combination with the rat β1 subunit and assessed the properties of the reconstituted channels by recording sodium currents using the whole-cell patch clamp technique. Coexpression with the β1 subunit accelerated the inactivation of sodium currents and shifted the voltage dependence of channel activation and steady-state fast inactivation by approximately 5-7 mV in the direction of depolarization. By contrast the β1 subunit had no effect on the stability of sodium currents following repeated depolarizations at high frequencies. Our results define modulatory effects of the β1 subunit on the properties of rat Nav1.6-mediated sodium currents reconstituted in HEK293 cells that differ from effects measured previously in the Xenopus oocyte expression system. We also identify differences in the kinetic and gating properties of the rat Nav1.6 channel expressed in the absence of the β1 subunit compared to the properties of the orthologous mouse and human channels expressed in this system.
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