ArticleJournal of neurophysiology2011
Regulation of Nav1.6 and Nav1.8 peripheral nerve Na+ channels by auxiliary β-subunits.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- The Excelsatoxin A-Receptor TMEM233 Modulates Nav1.8.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Immature olfactory sensory neurons are intrinsically excitable and show maturation-dependent changes in voltage-gated NaPflugers Archiv : European journal of physiology · 2026Article
- Distribution of Voltage-Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment.The Journal of comparative neurology · 2026Article
- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Structural basis of inhibition of human NaNature communications · 2025Article
- Tissue damage-induced axon injury-associated responses in sensory neurons: requirements, prevention, and potential role in persistent post-surgical pain.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Structural basis of inhibition of human NabioRxiv : the preprint server for biology · 2024Article
- Structure of human NaNature communications · 2023Article
- Cryo-EM structure of human voltage-gated sodium channel NaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Functional modulation of the human voltage-gated sodium channel NaChannels (Austin, Tex.) · 2021Article
- Resurgent NaNature communications · 2021Article
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- The Sodium Channel B4-Subunits are Dysregulated in Temporal Lobe Epilepsy Drug-Resistant Patients.International journal of molecular sciences · 2020Article
- Emerging roles for multifunctional ion channel auxiliary subunits in cancer.Cell calcium · 2019Review
- Loss-of-function of Nav1.8/D1639N linked to human pain can be rescued by lidocaine.Pflugers Archiv : European journal of physiology · 2018Article
- Effects of 4,9-anhydrotetrodotoxin on voltage-gated NaNaunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Cross-kingdom auxiliary subunit modulation of a voltage-gated sodium channel.The Journal of biological chemistry · 2018Article
- Voltage-gated sodium channel β subunits: The power outside the pore in brain development and disease.Neuropharmacology · 2018Review
- Roles of NaPflugers Archiv : European journal of physiology · 2018Review
- Puerarin Relieves Paclitaxel-Induced Neuropathic Pain: The Role of NaFrontiers in pharmacology · 2018Article
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3 authors.
Funding
Abstract
Voltage-gated Na(+) (Na(v)) channels are composed of a pore-forming α-subunit and one or more auxiliary β-subunits. The present study investigated the regulation by the β-subunit of two Na(+) channels (Na(v)1.6 and Na(v)1.8) expressed in dorsal root ganglion (DRG) neurons. Single cell RT-PCR was used to show that Na(v)1.8, Na(v)1.6, and β(1)-β(3) subunits were widely expressed in individually harvested small-diameter DRG neurons. Coexpression experiments were used to assess the regulation of Na(v)1.6 and Na(v)1.8 by β-subunits. The β(1)-subunit induced a 2.3-fold increase in Na(+) current density and hyperpolarizing shifts in the activation (-4 mV) and steady-state inactivation (-4.7 mV) of heterologously expressed Na(v)1.8 channels. The β(4)-subunit caused more pronounced shifts in activation (-16.7 mV) and inactivation (-9.3 mV) but did not alter the current density of cells expressing Na(v)1.8 channels. The β(3)-subunit did not alter Na(v)1.8 gating but significantly reduced the current density by 31%. This contrasted with Na(v)1.6, where the β-subunits were relatively weak regulators of channel function. One notable exception was the β(4)-subunit, which induced a hyperpolarizing shift in activation (-7.6 mV) but no change in the inactivation or current density of Na(v)1.6. The β-subunits differentially regulated the expression and gating of Na(v)1.8 and Na(v)1.6. To further investigate the underlying regulatory mechanism, β-subunit chimeras containing portions of the strongly regulating β(1)-subunit and the weakly regulating β(2)-subunit were generated. Chimeras retaining the COOH-terminal domain of the β(1)-subunit produced hyperpolarizing shifts in gating and increased the current density of Na(v)1.8, similar to that observed for wild-type β(1)-subunits. The intracellular COOH-terminal domain of the β(1)-subunit appeared to play an essential role in the regulation of Na(v)1.8 expression and gating.
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