Evidence map›Paper›PMID 16388111›Full record

ReviewMolecular neurobiology2006

The Role of Intracellular Sodium in the Regulation of NMDA-Receptor-Mediated Channel Activity and Toxicity.

Xian-Min Yu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Bicarbonate-Independent Sodium Conductance of Na/HCOCurrent issues in molecular biology · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Na,K-ATPase activity regulates AMPA receptor turnover through proteasome-mediated proteolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  17. Sodium channel activation augments NMDA receptor function and promotes neurite outgrowth in immature cerebrocortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  18. Activity-dependent neuronal cell migration induced by electrical stimulation.Medical & biological engineering & computing · 2009
    Article
  19. Article
  20. Influence of lipid-soluble gating modifier toxins on sodium influx in neocortical neurons.The Journal of pharmacology and experimental therapeutics · 2008
    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

1 author at 1 institution in 1 country.

Xian-Min YuDepartment of Biomedical Science, College of Medicine, Florida State University, Tallahassee, FL, USA. xianmin.yu@med.fsu.edu
Florida State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium (Na+) is the major cation in extracellular space and, with its entry into cells, may act as a critical intracellular second messenger that regulates many cellular functions. Through our investigations of mechanisms underlying the activity-dependent regulation of N-methyl-D-aspartate (NMDA) receptors, we recently characterized intracellular Na+ as a possible signaling factor common to processes underlying the upregulation of NMDA receptors by non-NMDA glutamate channels, voltage-gated Na+ channels, and remote NMDA receptors. Furthermore, although Ca2+ influx during the activation of NMDA receptors acts as a negative feedback mechanism that downregulates NMDA receptor activity, Na+ influx provides an essential positive feedback mechanism to overcome Ca2+ -induced inhibition, thereby potentiating both NMDA receptor activity and inward Ca2+ flow. NMDA receptors may be recruited to cause excitoxicity through a Na+ -dependent mechanism. Therefore, the further characterization of mechanisms underlying the regulation of NMDA receptors by intracellular Na+ is essential to understanding activity-dependent neuroplasticity in the nervous system.

Indexed as

AnimalsCalcium ChannelsCalcium SignalingCentral Nervous SystemHumansIntracellular FluidIon Channel GatingIon ChannelsNeuronsNeurotoxinsReceptors, N-Methyl-D-AspartateSodiumSodium ChannelsCalcium ChannelsIon ChannelsNeurotoxinsReceptors, N-Methyl-D-AspartateSodiumSodium Channels

Identifiers

PMID16388111
OpenAlexW2021456078

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.