ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Gating properties of Na(v)1.7 and Na(v)1.8 peripheral nerve sodium channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Electrostatic tuning of NaThe Journal of physiology · 2026Article
- Botulinum toxin type A attenuates trigeminal neuralgia-like pain by suppressing CGRP release and modulating NaV1.7-associated signaling.The journal of headache and pain · 2026Article
- From ion channel biology to clinical practice: suzetrigine as a precision analgesic.Frontiers in medicine · 2026Review
- Immunomodulatory functions of growth differentiation factor 15 in skin aging and inflammatory dermatoses.Frontiers in immunology · 2026Review
- Promoter demethylation of cerebellin 2 by ten-eleven translocation 3 contributes to peripheral sensitization in trigeminal neuropathic pain of mice.The journal of headache and pain · 2025Article
- Assessing NaV1.7 during tonic firing in pig C-nociceptors.PloS one · 2025Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Article
- Bioelectronic Medicine: a multidisciplinary roadmap from biophysics to precision therapies.Frontiers in integrative neuroscience · 2024Review
- Structural basis for high-voltage activation and subtype-specific inhibition of human NaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- N-type fast inactivation of a eukaryotic voltage-gated sodium channel.Nature communications · 2022Article
- Structural Advances in Voltage-Gated Sodium Channels.Frontiers in pharmacology · 2022Review
- Functional modulation of the human voltage-gated sodium channel NaChannels (Austin, Tex.) · 2021Article
- Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons.Neuroscience bulletin · 2021Article
- A Novel Spider Toxin Inhibits Fast Inactivation of the NaFrontiers in pharmacology · 2021Article
- Overexpressed NaFrontiers in cellular neuroscience · 2021Article
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Co-expression of β Subunits with the Voltage-Gated Sodium Channel NaJournal of molecular neuroscience : MN · 2018Article
- Different role of TTX-sensitive voltage-gated sodium channel (NaThe Journal of physiology · 2018Article
- Roles of NaPflugers Archiv : European journal of physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Several distinct components of voltage-gated sodium current have been recorded from native dorsal root ganglion (DRG) neurons that display differences in gating and pharmacology. This study compares the electrophysiological properties of two peripheral nerve sodium channels that are expressed selectively in DRG neurons (Na(v)1.7 and Na(v)1.8). Recombinant Na(v)1.7 and Na(v)1.8 sodium channels were coexpressed with the auxiliary beta(1) subunit in Xenopus oocytes. In this system coexpression of the beta(1) subunit with Na(v)1.7 and Na(v)1.8 channels results in more rapid inactivation, a shift in midpoints of steady-state activation and inactivation to more hyperpolarizing potentials, and an acceleration of recovery from inactivation. The coinjection of beta(1) subunit also significantly increases the expression of Na(v)1.8 by sixfold but has no effect on the expression of Na(v)1.7. In addition, a great percentage of Na(v)1.8+beta(1) channels is observed to enter rapidly into the slow inactivated states, in contrast to Nav1.7+beta(1) channels. Consequently, the rapid entry into slow inactivation is believed to cause a frequency-dependent reduction of Na(v)1.8+beta(1) channel amplitudes, seen during repetitive pulsing between 1 and 2 Hz. However, at higher frequencies (>20 Hz) Na(v)1.8+beta(1) channels reach a steady state to approximately 42% of total current. The presence of this steady-state sodium channel activity, coupled with the high activation threshold (V(0.5) = -3.3 mV) of Na(v)1.8+beta(1), could enable the nociceptive fibers to fire spontaneously after nerve injury.
Indexed as
Identifiers
11588164PMC6763856W1982950553What 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.