Evidence map›Paper›PMID 19279266›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Sodium channel activation augments NMDA receptor function and promotes neurite outgrowth in immature cerebrocortical neurons.

Joju George, Shashank M Dravid, Anand Prakash, Jun Xie, Jennifer Peterson, Sairam V Jabba, Daniel G Baden, Thomas F Murray

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Neurexin-1α regulates neurite growth of rat hippocampal neurons.International journal of physiology, pathophysiology and pharmacology · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Bidirectional influence of sodium channel activation on NMDA receptor-dependent cerebrocortical neuron structural plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. Article
  18. 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

8 authors at 4 institutions in 2 countries.

Joju GeorgeDepartment of Pharmacology, Creighton University School of Medicine, Omaha, Nebraska 68178, USA.
Shashank M Dravid
Anand Prakash
Jun Xie
Jennifer Peterson
Sairam V Jabba
Daniel G Baden
Thomas F Murray
Creighton University · USShanxi Medical University · CNUniversity of Georgia · USUniversity of North Carolina Wilmington · US

Funding

The Respiratory Eff. Study of Aerosolized Red Tide Toxins in HumansP01ES010594 · NIEHS · UNIVERSITY OF NORTH CAROLINA WILMINGTON · PI BADEN, DANIEL G · 2000 to 2011
$15.2M
Neurotoxins from Marine Algae and CyanobacteriaR01NS053398 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GERWICK, WILLIAM HENRY, MURRAY, THOMAS F · 2005 to 2015
$4.3M
NIEHS NIH HHS ES10594NIEHS NIH HHS P01 ES010594NINDS NIH HHS NS053398NINDS NIH HHS R01 NS053398
6 · The paper itself

Abstract

A range of extrinsic signals, including afferent activity, affect neuronal growth and plasticity. Neuronal activity regulates intracellular Ca(2+), and activity-dependent calcium signaling has been shown to regulate dendritic growth and branching (Konur and Ghosh, 2005). NMDA receptor (NMDAR) stimulation of Ca(2+)/calmodulin-dependent protein kinase signaling cascades has, moreover, been demonstrated to regulate neurite/axonal outgrowth (Wayman et al., 2004). We used a sodium channel activator, brevetoxin (PbTx-2), to explore the relationship between intracellular [Na(+)] and NMDAR-dependent development. PbTx-2 alone, at a concentration of 30 nM, did not affect Ca(2+) dynamics in 2 d in vitro cerebrocortical neurons; however, this treatment robustly potentiated NMDA-induced Ca(2+) influx. The 30 nM PbTx-2 treatment produced a maximum [Na(+)](i) of 16.9 +/- 1.5 mM, representing an increment of 8.8 +/- 1.8 mM over basal. The corresponding membrane potential change produced by 30 nM PbTx-2 was modest and, therefore, insufficient to relieve the voltage-dependent Mg(2+) block of NMDARs. To unambiguously demonstrate the enhancement of NMDA receptor function by PbTx-2, we recorded single-channel currents from cell-attached patches. PbTx-2 treatment was found to increase both the mean open time and open probability of NMDA receptors. These effects of PbTx-2 on NMDA receptor function were dependent on extracellular Na(+) and activation of Src kinase. The functional consequences of PbTx-2-induced enhancement of NMDAR function were evaluated in immature cerebrocortical neurons. PbTx-2 concentrations between 3 and 300 nM enhanced neurite outgrowth. Voltage-gated sodium channel activators may accordingly represent a novel pharmacologic strategy to regulate neuronal plasticity through an NMDA receptor and Src family kinase-dependent mechanism.

Indexed as

AnimalsCells, CulturedCerebral CortexFemaleMarine ToxinsMembrane PotentialsMiceNeuritesNeuronsOxocinsPolyether ToxinsPregnancyReceptors, N-Methyl-D-AspartateSodium Channel AgonistsSodium ChannelsbrevetoxinMarine ToxinsOxocinsPolyether ToxinsReceptors, N-Methyl-D-AspartateSodium Channel AgonistsSodium Channels

Identifiers

PMID19279266
PMCPMC2683593
OpenAlexW2084002376

What OpenQuestion holds

Textmetadata
LicenceTDM
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.