Evidence map›Paper›PMID 25168337›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2015

Extrasynaptic NMDA Receptor in Excitotoxicity: Function Revisited.

Xianju Zhou, Zhuoyou Chen, Wenwei Yun, Jianhua Ren, Chengwei Li, Hongbing Wang

Open access · greenAbstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Synaptic and extrasynaptic distribution of NMDA receptors in the cortex of Alzheimer's disease patients.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  4. Review
  5. Article
  6. The NMDA receptor antagonists memantine and ketamine as anti-migraine agents.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
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  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

6 authors at 4 institutions in 2 countries.

Xianju ZhouDepartment of Neurology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, China.
Zhuoyou ChenDepartment of Neurology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, China.
Wenwei YunDepartment of Neurology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, China.
Jianhua RenKey Laboratory of Translational Neuroscience, Zhoukou Normal University, Zhoukou China.
Chengwei LiCollege of Life Science and Agronomy, Zhoukou Normal University, Zhoukou China.
Hongbing WangDepartment of Physiology and Neuroscience Program, Michigan State University, East Lansing, MI, USA hippocampus2007@gmail.com wangho@msu.edu.
Nanjing Medical University · CNZhoukou Normal University · CNChangzhou No.2 People's Hospital · CNMichigan State University · US

Funding

Connecting mGluR and cAMP in the pre-clinical model of Fragile XR01MH093445 · NIMH · MICHIGAN STATE UNIVERSITY · PI WANG, HONGBING · 2012 to 2016
$1.9M
Function and Property of Extrasynaptic NMDAR in Neuronal Cell DeathR03NS072668 · NINDS · MICHIGAN STATE UNIVERSITY · PI WANG, HONGBING · 2010 to 2011
$140k
NIMH NIH HHS MH093445NIMH NIH HHS R01 MH093445NINDS NIH HHS NS072668NINDS NIH HHS R03 NS072668
6 · The paper itself

Abstract

It is generally accepted that proper activation of N-methyl-d-aspartate receptors (NMDARs) promotes neuronal survival and supports neuroplasticity, and excessive NMDAR activation leads to pathological outcomes and neurodegeneration. As NMDARs are found at both synaptic and extrasynaptic sites, there is significant interest in determining how NMDARs at different subcellular locations differentially regulate physiological as well as pathological functions. Better understanding of this issue may support the development of therapeutic strategies to attenuate neuronal death or promote normal brain function. Although the current prevailing theory emphasizes the major role of extrasynaptic NMDARs in neurodegeneration, there is growing evidence indicating the involvement of synaptic receptors. It is also evident that physiological functions of the brain also involve extrasynaptic NMDARs. Our recent studies demonstrate that the degree of cell death following neuronal insults depends on the magnitude and duration of synaptic and extrasynaptic receptor co-activation. These new results underscore the importance of revisiting the function of extrasynaptic NMDARs in cell fate. Furthermore, the development of antagonists that preferentially inhibit synaptic or extrasynaptic receptors may better clarify the role of NMDARs in neurodegeneration.

Indexed as

AnimalsBrainCell DeathHumansNeurodegenerative DiseasesNeuronsReceptors, N-Methyl-D-AspartateSynapsesReceptors, N-Methyl-D-Aspartatecalciumexcitotoxicityextrasynaptic NMDARneurodegenerationsynaptic NMDAR

Identifiers

PMID25168337
PMCPMC4620718
OpenAlexW1994419985

What OpenQuestion holds

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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.