Evidence map›Paper›PMID 22855776›Full record

ArticleJournal of neurophysiology2012

Tetrodotoxin-resistant voltage-dependent sodium channels in identified muscle afferent neurons.

Renuka Ramachandra, Stephanie Y McGrew, James C Baxter, Esad Kiveric, Keith S Elmslie

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. NaJournal of neurophysiology · 2022
    Article
  3. KJournal of neurophysiology · 2021
    Article
  4. Enhancement by TNF-α of TTX-resistant NaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  5. Article
  6. Loss-of-function of Nav1.8/D1639N linked to human pain can be rescued by lidocaine.Pflugers Archiv : European journal of physiology · 2018
    Article
  7. NaJournal of neurophysiology · 2018
    Article
  8. Article
  9. Article
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  14. Role played by NaV 1.7 channels on thin-fiber muscle afferents in transmitting the exercise pressor reflex.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Article
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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

5 authors at 1 institution in 1 country.

Renuka RamachandraThe Baker Laboratory of Pharmacology, Department of Pharmacology, Kirksville College of Osteopathic Medicine, AT Still University of Health Sciences, Kirksville, MO 63501, USA.
Stephanie Y McGrew
James C Baxter
Esad Kiveric
Keith S Elmslie
A.T. Still University · US

Funding

Excitability of Afferents Evoking the Exercise Pressor ReflexR01AR059397 · NIAMS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI ELMSLIE, KEITH S, KAUFMAN, MARC PETER · 2010 to 2019
$5.4M
NIAMS NIH HHS AR-059397NIAMS NIH HHS R01 AR059397
6 · The paper itself

Abstract

Muscle afferents are critical regulators of motor function (Group I and II) and cardiovascular responses to exercise (Group III and IV). However, little is known regarding the expressed voltage-dependent ion channels. We identified muscle afferent neurons in dorsal root ganglia (DRGs), using retrograde labeling to examine voltage-dependent sodium (Na(V)) channels. In patch-clamp recordings, we found that the dominant Na(V) current in the majority of identified neurons was insensitive to tetrodotoxin (TTX-R), with Na(V) current in only a few (14%) neurons showing substantial (>50%) TTX sensitivity (TTX-S). The TTX-R current was sensitive to a Na(V)1.8 channel blocker, A803467. Immunocytochemistry demonstrated labeling of muscle afferent neurons by a Na(V)1.8 antibody, which further supported expression of these channels. A portion of the TTX-R Na(V) current appeared to be noninactivating during our 25-ms voltage steps, which suggested activity of Na(V)1.9 channels. The majority of the noninactivating current was insensitive to A803467 but sensitive to extracellular sodium. Immunocytochemistry showed labeling of muscle afferent neurons by a Na(V)1.9 channel antibody, which supports expression of these channels. Further examination of the muscle afferent neurons showed that functional TTX-S channels were expressed, but were largely inactivated at physiological membrane potentials. Immunocytochemistry showed expression of the TTX-S channels Na(V)1.6 and Na(V)1.7 but not Na(V)1.1. Na(V)1.8 and Na(V)1.9 appear to be the dominant functional sodium channels in small- to medium-diameter muscle afferent neurons. The expression of these channels is consistent with the identification of these neurons as Group III and IV, which mediate the exercise pressor reflex.

Indexed as

Action PotentialsAniline CompoundsAnimalsFuransGanglia, SpinalGene ExpressionMaleMuscle, SkeletalNeurons, AfferentRatsRats, Sprague-DawleySodiumTetrodotoxinVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium ChannelsA 803467Aniline CompoundsFuransSodiumTetrodotoxinVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium Channels

Identifiers

PMID22855776
PMCPMC3545019
OpenAlexW2089842487

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.