Evidence map›Paper›PMID 7897490›Full record

ArticleJournal of neurophysiology1994

Slow sodium conductances of dorsal root ganglion neurons: intraneuronal homogeneity and interneuronal heterogeneity.

M A Rizzo, J D Kocsis, S G Waxman

Open access · greenAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Sodium channels and pain: from toxins to therapies.British journal of pharmacology · 2018
    Review
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  5. Article
  6. Review
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  11. 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 · 2010
    Article
  12. Article
  13. Article
  14. Article
  15. Review
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  18. 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 · 2006
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

M A RizzoDepartment of Neurology, Yale University School of Medicine, New Haven 06510.
J D Kocsis
S G Waxman
Yale University · US

Funding

REORGANIZATION OF AXONAL TRACTS FOLLOWING TRANSECTIONP50NS010174 · NINDS · YALE UNIVERSITY · PI COLLINS, WILLIAM F · 1985 to 2002
$2.8M
NINDS NIH HHS P50 NS010174
6 · The paper itself

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)

Indexed as

AnimalsCations, DivalentCells, CulturedCesiumGanglia, SpinalIon Channel GatingKineticsMaleNeuronsPatch-Clamp TechniquesRatsRats, WistarSodium ChannelsTetrodotoxinCations, DivalentCesiumSodium ChannelsTetrodotoxin

Identifiers

PMID7897490
PMCPMC2605955
OpenAlexW1661274927

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.