ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Role of tetrodotoxin-resistant Na+ current slow inactivation in adaptation of action potential firing in small-diameter dorsal root ganglion neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
80 citing papers in PubMed, 161 citations in OpenAlex.
- Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.The Journal of physiology · 2026Article
- The Excelsatoxin A-Receptor TMEM233 Modulates Nav1.8.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Suzetrigine, a NaMolecules (Basel, Switzerland) · 2026Review
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Differential state-dependent Nav1.8 inhibition by suzetrigine, LTGO-33, and A-887826.The Journal of general physiology · 2025Article
- Inhibiting Nav1.8 for pain: Lessons from patients and from neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The analgesic paracetamol metabolite AM404 acts peripherally to directly inhibit sodium channels.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Modulation of human dorsal root ganglion neuron firing by the Nav1.8 inhibitor suzetrigine.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Sodium channel slow inactivation normalizes firing in axons with uneven conductance distributions.Current biology : CB · 2023Article
- Use-Dependent Relief of Inhibition of Nav1.8 Channels by A-887826.Molecular pharmacology · 2023Article
- Contribution of tetrodotoxin-resistant persistent NaThe journal of headache and pain · 2022Article
- Multitarget nociceptor sensitization by a promiscuous peptide from the venom of the King Baboon spider.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Non-psychotropic phytocannabinoid interactions with voltage-gated sodium channels: An update on cannabidiol and cannabigerol.Frontiers in physiology · 2022Review
- Structural and Functional Characterization of a Novel Scorpion Toxin that Inhibits NaFrontiers in pharmacology · 2022Article
- Cannabidiol Inhibition of Murine Primary Nociceptors: Tight Binding to Slow Inactivated States of NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The Input-Output Relation of Primary Nociceptive Neurons is Determined by the Morphology of the Peripheral Nociceptive Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- An Index Combining Lost and Remaining Nerve Fibers Correlates with Pain Hypersensitivity in Mice.Cells · 2020Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
When acutely dissociated small-diameter dorsal root ganglion (DRG) neurons were stimulated with repeated current injections or prolonged application of capsaicin, their action potential firing quickly adapted. Because TTX-resistant (TTX-R) sodium current in these presumptive nociceptors generates a large fraction of depolarizing current during the action potential, we examined the possible role of inactivation of TTX-R sodium channels in producing adaptation. Under voltage clamp, TTX-R current elicited by short depolarizations showed strong use dependence at frequencies as low as 1 Hz, although recovery from fast inactivation was complete in approximately 10-30 msec. This use-dependent reduction was the result of the entry of TTX-R sodium channels into slow inactivated states. Slow inactivation was more effectively produced by steady depolarization than by cycling channels through open states. Slow inactivation was steeply voltage dependent, with a Boltzmann slope factor of 5 mV, a midpoint near -45 mV (5 sec conditioning pulses), and completeness of approximately 93% positive to -20 mV. The time constant for entry (approximately 200 msec) was independent of voltage from -20 mV to +60 mV, whereas recovery kinetics were moderately voltage dependent (time constant, approximately 1.5 sec at -60 mV and approximately 0.5 sec at -100 mV). Using a prerecorded current-clamp response to capsaicin as a voltage-clamp command waveform, we found that adaptation of firing occurred with a time course similar to that of development of slow inactivation. Thus, slow inactivation of the TTX-R sodium current limits the duration of small DRG cell firing in response to maintained stimuli and may contribute to cross desensitization between chemical and electrical stimuli.
Indexed as
Identifiers
14614093PMC6741008W1531283035What 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.