ArticleMolecular pain2007
Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization.
Article in Molecular pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.The Journal of physiology · 2026Article
- T-World Virtual Human Cardiomyocyte. II. Organ-Scale Simulations and Applications.Circulation research · 2026Article
- The Chemistry and Biology of the Tetrodotoxin Natural Product Family.Angewandte Chemie (International ed. in English) · 2025Review
- 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
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- Electrophysiological Alterations Driving Pain-Associated Spontaneous Activity in Human Sensory Neuron Somata Parallel Alterations Described in Spontaneously Active Rodent Nociceptors.The journal of pain · 2022Article
- The Potential Effect of NaFrontiers in molecular neuroscience · 2021Article
- Adaptive mechanisms driving maladaptive pain: how chronic ongoing activity in primary nociceptors can enhance evolutionary fitness after severe injury.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- The functional consequences of sodium channel NaESC heart failure · 2019Article
- Article
- Modulation of sodium channels as pharmacological tool for pain therapy-highlights and gaps.Naunyn-Schmiedeberg's archives of pharmacology · 2018Review
- Atypical changes in DRG neuron excitability and complex pain phenotype associated with a NaScientific reports · 2018Article
- The NaFrontiers in pharmacology · 2018Review
- Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability.The Journal of clinical investigation · 2017Article
- Sodium channel diversity in the vestibular ganglion: NaV1.5, NaV1.8, and tetrodotoxin-sensitive currents.Journal of neurophysiology · 2016Article
- Angiotensin II-superoxide-NFκB signaling and aortic baroreceptor dysfunction in chronic heart failure.Frontiers in neuroscience · 2015Review
- Sodium channels and mammalian sensory mechanotransduction.Molecular pain · 2012Article
- TRPA1 contributes to specific mechanically activated currents and sensory neuron mechanical hypersensitivity.The Journal of physiology · 2011Article
- Reduced expression and activation of voltage-gated sodium channels contributes to blunted baroreflex sensitivity in heart failure rats.Journal of neuroscience research · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSmall neurons of the dorsal root ganglion (DRG) express five of the nine known voltage-gated sodium channels. Each channel has unique biophysical characteristics which determine how it contributes to the generation of action potentials (AP). To better understand how AP amplitude is maintained in nociceptive DRG neurons and their centrally projecting axons, which are subjected to depolarization within the dorsal horn, we investigated the dependence of AP amplitude on membrane potential, and how that dependence is altered by the presence or absence of sodium channel Nav1.8.
resultsIn small neurons cultured from wild type (WT) adult mouse DRG, AP amplitude decreases as the membrane potential is depolarized from -90 mV to -30 mV. The decrease in amplitude is best fit by two Boltzmann equations, having V1/2 values of -73 and -37 mV. These values are similar to the V1/2 values for steady-state fast inactivation of tetrodotoxin-sensitive (TTX-s) sodium channels, and the tetrodotoxin-resistant (TTX-r) Nav1.8 sodium channel, respectively. Addition of TTX eliminates the more hyperpolarized V1/2 component and leads to increasing AP amplitude for holding potentials of -90 to -60 mV. This increase is substantially reduced by the addition of potassium channel blockers. In neurons from Nav1.8(-/-) mice, the voltage-dependent decrease in AP amplitude is characterized by a single Boltzmann equation with a V1/2 value of -55 mV, suggesting a shift in the steady-state fast inactivation properties of TTX-s sodium channels. Transfection of Nav1.8(-/-) DRG neurons with DNA encoding Nav1.8 results in a membrane potential-dependent decrease in AP amplitude that recapitulates WT properties.
conclusionWe conclude that the presence of Nav1.8 allows AP amplitude to be maintained in DRG neurons and their centrally projecting axons even when depolarized within the dorsal horn.
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