ArticleJournal of neurophysiology1994
Slow sodium conductances of dorsal root ganglion neurons: intraneuronal homogeneity and interneuronal heterogeneity.
Article in Journal of neurophysiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 125 citations in OpenAlex.
- Dorsal root ganglion neurons recapitulate the traumatic axonal injury of CNS neurons in response to a rapid stretchFrontiers in cellular neuroscience · 2023Article
- Sodium channels and pain: from toxins to therapies.British journal of pharmacology · 2018Review
- Tolerance to Morphine-Induced Inhibition of TTX-R Sodium Channels in Dorsal Root Ganglia Neurons Is Modulated by Gut-Derived Mediators.iScience · 2018Article
- Article
- Nonlinear effects of hyperpolarizing shifts in activation of mutant NaJournal of neurophysiology · 2017Article
- Review
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
- Advanced Genetic Testing Comes to the Pain Clinic to Make a Diagnosis of Paroxysmal Extreme Pain Disorder.Case reports in neurological medicine · 2016Article
- EXPRESS: Voltage-dependent sodium (NaV) channels in group IV sensory afferents.Molecular pain · 2016Article
- Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.Journal of neurophysiology · 2015Article
- ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable.Molecular pain · 2008Article
- Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization.Molecular pain · 2007Article
- Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.The Journal of physiology · 2007Review
- Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Article
- A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Schwann cell engraftment into injured peripheral nerve prevents changes in action potential properties.Journal of neurophysiology · 2005Article
- GTP gamma S increases Nav1.8 current in small-diameter dorsal root ganglia neurons.Experimental brain research · 2003Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Voltage-dependent Na+ conductances were studied in small (18-25 microns diam) adult rat dorsal root ganglion (DRG) neurons with the use of the whole cell patch-clamp technique. Na+ currents were also recorded from larger (44-50 microns diam) neurons and compared with those of the small neurons. 2. The predominant Na+ conductance in the small neurons was selective over tetramethylammonium by at least 10-fold and was resistant to 1 microM external tetrodotoxin (TTX). Na+ conductances in many larger DRG neurons were kinetically faster and, in contrast, were blocked by 1 microM TTX. 3. The Na+ conductance in the small neurons was kinetically slow. Activation half-times were voltage dependent and ranged from 2 ms at -20 mV to 0.7 ms at +50 mV. Approximately 50% of the activation half-time was comprised of an initial delay. Inactivation half-times were voltage dependent and ranged from 11 ms at -20 mV to 2 ms at +50 mV. 4. Peak slow Na+ conductances were near maximal with conditioning potentials negative to -120 mV and were significantly reduced or eliminated with conditioning potentials positive to -40 mV. The slow Na+ conductance increased gradually with test potentials extending from -40 to +40 mV. In some cells the conductance could be saturated at +10 mV. Peak conductance/voltage relationships, although stable in a given neuron, revealed marked variability among neurons, spanning > 20- and 50-mV domains for steady-state activation and inactivation (current availability), respectively. 5. Kinetics remained stable within a given neuron over the course of an experiment. However, considerable kinetic variation was exhibited from neuron to neuron, such that the half-times of activation and of inactivation spanned an order of magnitude. In all small neurons studied there appeared to be a singular kinetic component of the current, based on sensitivity to the conditioning potential, voltage dependence of activation, and inactivation half-time. 6. Unique closing properties were exhibited by Na+ channels of the small neurons. Hyperpolarization following a depolarization-induced fully inactivated state resulted in tail currents that appeared to be the consequence of reactivation of the slow Na+ conductance. Tail currents recorded at various times during a fixed level of depolarization revealed that the underlying channels accumulated into a volatile inactivated state over the course of the preceding depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)
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