Evidence map›Paper›PMID 24719102›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Specialized functions of Nav1.5 and Nav1.9 channels in electrogenesis of myenteric neurons in intact mouse ganglia.

Nancy Osorio, Sergiy Korogod, Patrick Delmas

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. T-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Article
  8. Article
  9. The Gain-of-Function R222S Variant inFrontiers in neurology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. The development of somatosensory neurons: Insights into pain and itch.Current topics in developmental biology · 2021
    Review
  14. Article
  15. Article
  16. Simulations of Myenteric Neuron Dynamics in Response to Mechanical Stretch.Computational intelligence and neuroscience · 2020
    Article
  17. Article
  18. Article
  19. Voltage-gated sodium channels: (NaThe Journal of physiology · 2018
    Review
  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 3 institutions in 2 countries.

Nancy OsorioAix-Marseille-Université, Centre National de la Recherche Scientifique, Centre de Recherche en Neurobiologie et Neurophysiologie de Marseille, Unité Mixte de Recherche 7286, 13344 Marseille France, and International Center for Molecular Physiology (Dnipropetrovsk Division), National Academy of Sciences of Ukraine, 01024 Kiev, Ukraine.
Sergiy Korogod
Patrick Delmas
Aix-Marseille Université · FRCentre National de la Recherche Scientifique · FRNational Metallurgical Academy of Ukraine · UA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated sodium (Nav) channels play a central role in gastrointestinal physiology because they transmit depolarizing impulses in enteric neurons, thereby enabling the coordination of intestinal motility. However, little is known about the ion channel machinery that specifies firing pattern of enteric neurons. Here, we used in situ patch-clamp recording of myenteric neurons from mice to define functionally the Nav channel subtypes responsible for the electrical signature of myenteric neurons. We found that mouse myenteric neurons exhibit two types of tetrodotoxin-resistant Na(+) currents: an early inactivating Na(+) current (INaT) and a persistent Na(+) current (INaP). INaT was encountered in all myenteric neurons, whereas INaP was preferentially found in Dogiel type II sensory neurons. Knock-out mouse studies, in combination with pharmacological assays, indicate that INaT is carried by the Scn5a-encoded "cardiac" Nav1.5, whereas INaP is attributed to the Scn11a-encoded Nav1.9. Current-clamp experiments show that Nav1.9 flows at subthreshold voltages, generating tonic firing. In addition, action potential (AP) clamp reveals that Nav1.5 contributes to the upstroke velocity of APs, whereas Nav1.9, which remains active during the falling phase, opposes AP repolarization. We developed a computational model of a Dogiel type II myenteric neuron that successfully reproduces all experimentally observed phenomena and highlights the differential roles of Nav1.5 and Nav1.9 in the control of excitability. Our data illustrate how excitability can be finely tuned to provide specific firing templates by the selective deployment of Nav1.5 and Nav1.9 isoforms. We propose that Nav-dependent ENS disorders of excitability may play important roles in the pathogenesis of digestive diseases.

Indexed as

Action PotentialsAnimalsMaleMiceMice, Inbred C57BLModels, NeurologicalMyenteric PlexusNAV1.5 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelProtein IsoformsSensory Receptor CellsSodium Channel BlockersTetrodotoxinNAV1.5 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelProtein IsoformsScn11a protein, mouseScn5a protein, mouseSodium Channel BlockersTetrodotoxinaction potentialsenteric neuronsexcitabilitygastrointestinal diseasein situ patch clampsodium channels

Identifiers

PMID24719102
PMCPMC6609004
OpenAlexW1985977003

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.