Evidence map›Paper›PMID 9651206›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons.

K D García, L K Sprunger, M H Meisler, K G Beam

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Trafficking mechanisms underlying NaChannels (Austin, Tex.) · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. The contribution of resurgent sodium current to high-frequency firing in Purkinje neurons: an experimental and modeling study.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Functional analysis of the mouse Scn8a sodium channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  17. 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

4 authors at 2 institutions in 1 country.

K D GarcíaDepartment of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523-1670, USA.
L K Sprunger
M H Meisler
K G Beam
Colorado State University · USUniversity of Michigan–Ann Arbor · US

Funding

The neuronal sodium channel gene SCN8AR01NS034509 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MIRIAM H MEISLER · 1996 to 2026
$9.5M
REGULATION OF MEMBRANE EXCITABILITYR01NS024444 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BEAM, KURT G · 1986 to 2005
$1.8M
MOLECULAR MECHANISM OF CARDIAC K+ CHANNEL INACTIVATIONK08HL002972 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI SPRUNGER, LESLIE K · 1994 to 1998
–
NHLBI NIH HHS HL02972NINDS NIH HHS NS24444NINDS NIH HHS NS34509NINDS NIH HHS R01 NS024444NINDS NIH HHS R01 NS034509
6 · The paper itself

Abstract

Sodium currents were recorded from motoneurons that were isolated from mice at postnatal days 0-8 (P0-P8) and maintained in culture for 12-24 hr. Motoneurons from normal mice exhibited a more than threefold increase in peak sodium current density from P0 to P8. For mice lacking a functional Scn8a sodium channel gene, motoneuronal sodium current density was comparable at P0 to that of normal mice but failed to increase from P0 to P8. The absence of Scn8a sodium channels is associated with the phenotype "motor end plate disease," which is characterized by a progressive neuromuscular failure and is fatal by 3-4 postnatal weeks. Thus, it appears that the development and function of mature motoneurons depends on the postnatal induction of Scn8a expression.

Indexed as

AnimalsAnimals, NewbornMiceMice, Inbred C3HMice, TransgenicMotor NeuronsRNA, MessengerSodium ChannelsSpinal CordRNA, MessengerSodium Channels

Identifiers

PMID9651206
PMCPMC6793491
OpenAlexW1921512660

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.