Evidence map›Paper›PMID 11007874›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Transient NMDA receptor inactivation provides long-term protection to cultured cortical neurons from a variety of death signals.

R Tremblay, B Chakravarthy, K Hewitt, J Tauskela, P Morley, T Atkinson, J P Durkin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-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

26 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
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  7. Article
  8. Calpain-1 contributes to IgE-mediated mast cell activation.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
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  13. Review
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  15. Aβ internalization by neurons and glia.International journal of Alzheimer's disease · 2011
    Article
  16. Article
  17. Article
  18. Article
  19. Pharmacodynamics of memantine: an update.Current neuropharmacology · 2008
    Article
  20. Killer proteases and little strokes--how the things that do not kill you make you stronger.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2007
    Review
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

7 authors at 2 institutions in 2 countries.

R TremblayInstitute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada K1A 0R6.
B Chakravarthy
K Hewitt
J Tauskela
P Morley
T Atkinson
J P Durkin
Institute for Biological Sciences · CANational Academies of Sciences, Engineering, and Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NMDA receptor antagonists, such as (+)-5-methyl-10, 11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate (MK-801), potently block glutamate-induced neuronal death in myriad in vitro cell models and effectively attenuate ischemic damage in vivo. In this report, a novel role for MK-801 and other NMDA receptor antagonists in preconditioning neurons to withstand a wide range of subsequent lethal insults is described. A brief 30 min exposure to 0.1 microM MK-801, applied up to 96 hr before a "lethal" insult, protected primary cortical neurons from a diverse group of neurotoxic agents, including NMDA, beta-amyloid, staurosporine, etoposide, and oxygen-glucose deprivation. This neuroprotective preconditioning by MK-801 arose from transient NMDA receptor inactivation, because the noncompetitive NMDA receptor antagonists memantine and nylindin and the competitive antagonist AP-5 gave similar effects. MK-801 protection was dependent on new protein synthesis during the first 2 hr, but not from 2 to 5 hr, after MK-801 exposure. The MK-801 transient did not alter the ability of NMDA to trigger normally lethal [Ca(2+)](i) influx 48 hr later, but it did block early downstream signaling events coupled to NMDA neurotoxicity, including PKC inactivation and the activation of calpain. Moreover, MK-801 protected neurons from staurosporine-induced apoptosis, although caspase activation in these cells was unimpeded. It is likely that the stress associated with transient inactivation of NMDA receptors triggered a rapid compensatory survival response that provided long-term protection from a spectrum of insults, inducing apoptotic and nonapoptotic death. The possibility that MK-801 preconditioning blocks an event common to seemingly diverse death mechanisms suggests it will be an important tool for obtaining a clearer understanding of the salient molecular events at work in neuronal death and survival pathways.

Indexed as

Adrenergic beta-AgonistsAnimalsApoptosisCalciumCalpainCell DeathCells, CulturedCell SurvivalCerebral CortexEnzyme InhibitorsExcitatory Amino Acid AntagonistsGlucoseHypoxia, BrainIschemic PreconditioningNeuronsNeuroprotective AgentsAdrenergic beta-AgonistsCalciumCalpainEnzyme InhibitorsExcitatory Amino Acid AntagonistsGlucoseNeuroprotective AgentsNeurotoxinsN-MethylaspartateProtein Kinase CProtein Synthesis InhibitorsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID11007874
PMCPMC6772776
OpenAlexW1625998218

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.