Evidence map›Paper›PMID 11487629›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Activation of metabotropic glutamate receptor 1 accelerates NMDA receptor trafficking.

J Y Lan, V A Skeberdis, T Jover, X Zheng, M V Bennett, R S Zukin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
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  5. Review
  6. Mechanism for neurotransmitter-receptor matching.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Identification of the SNARE complex mediating the exocytosis of NMDA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Downregulation of Src-kinase and glutamate-receptor phosphorylation after traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    Article
  18. Article
  19. Review
  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 1 institution in 1 country.

J Y LanDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
V A Skeberdis
T Jover
X Zheng
M V Bennett
R S Zukin
Albert Einstein College of Medicine · US

Funding

PURIFICATION OF NEUROBLASTOMA OPIATE RECEPTORSR01NS020752 · NINDS · YESHIVA UNIVERSITY · PI ZUKIN, R. SUZANNE · 1985 to 2009
$3.6M
GLUTAMATE RECEPTOR GENE EXPRESSION IN ISCHEMIAR01NS031282 · NINDS · YESHIVA UNIVERSITY · PI ZUKIN, R. SUZANNE · 1996 to 2000
$574k
NINDS NIH HHS NS 07512NINDS NIH HHS NS 20752NINDS NIH HHS NS 31282NINDS NIH HHS R01 NS020752
6 · The paper itself

Abstract

Regulation of neuronal NMDA receptors (NMDARs) by group I metabotropic glutamate receptors (mGluRs) is known to play a critical role in synaptic transmission. The molecular mechanisms underlying mGluR1-mediated potentiation of NMDARs are as yet unclear. The present study shows that in Xenopus oocytes expressing recombinant receptors, activation of mGluR1 potentiates NMDA channel activity by recruitment of new channels to the plasma membrane via regulated exocytosis. Activation of mGluR1alpha induced (1) an increase in channel number times channel open probability, with no change in mean open time, unitary conductance, or reversal potential; (2) an increase in charge transfer in the presence of NMDA and the open channel blocker MK-801, indicating an increased number of functional NMDARs in the cell membrane; and (3) increased NR1 surface expression, as indicated by cell surface Western blots and immunofluorescence. Botulinum neurotoxin A or expression of a dominant negative mutant of synaptosomal associated protein of 25 kDa molelcular mass (SNAP-25) greatly reduced mGluR1alpha-mediated potentiation, indicating that receptor trafficking occurs via a SNAP-25-mediated form of soluble N-ethylmaleimide sensitive fusion protein attachment protein receptor-dependent exocytosis. Because group I mGluRs are localized to the perisynaptic region in juxtaposition to synaptic NMDARs at glutamatergic synapses in the hippocampus, mGluR-mediated insertion of NMDARs may play a role in synaptic transmission and plasticity, including long-term potentiation.

Indexed as

Membrane ProteinsAnimalsBlotting, WesternBotulinum Toxins, Type ACell MembraneCells, CulturedCycloleucineDizocilpine MaleateExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsExocytosisFluorescent Antibody TechniqueIon Channel GatingMembrane PotentialsNerve Tissue ProteinsN-Methylaspartate1-amino-1,3-dicarboxycyclopentaneBotulinum Toxins, Type ACycloleucineDizocilpine MaleateExcitatory Amino Acid AgonistsExcitatory Amino Acid AntagonistsMembrane Proteinsmetabotropic glutamate receptor type 1Nerve Tissue ProteinsN-MethylaspartateNR1 NMDA receptorNR2A NMDA receptorReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateSnap25 protein, ratSynaptosomal-Associated Protein 25

Identifiers

PMID11487629
PMCPMC6763135
OpenAlexW1674210262

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.