Evidence map›Paper›PMID 25348411›Full record

ArticleThe Journal of general physiology2014

Extracellular Ca(2+) ions reduce NMDA receptor conductance and gating.

Bruce A Maki, Gabriela K Popescu

Open access · greenAbstract read
In one paragraph

Article in The Journal of general physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Dynamic control of NMDA receptor CaProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Estimating the CaMethods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Estimating the CaMethods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Membrane Stretch Gates NMDA Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. CaBiophysical journal · 2020
    Article
  18. Review
  19. Article
  20. Spatial Coupling Tunes NMDA Receptor Responses via CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    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

2 authors at 1 institution in 1 country.

Bruce A MakiDepartment of Biochemistry and Neuroscience Program, School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14214.
Gabriela K PopescuDepartment of Biochemistry and Neuroscience Program, School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14214 Department of Biochemistry and Neuroscience Program, School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14214 popescu@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Probing allosteric surfaces of NMDA receptorsR01NS052669 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI POPESCU, GABRIELA K · 2006 to 2015
$3.4M
Gating Mechanism of NMDA ReceptorsR01NS108750 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI POPESCU, GABRIELA K · 2019 to 2023
$1.5M
Permeation Mechanisms in NMDA receptorsR01NS097016 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI POPESCU, GABRIELA K · 2016 to 2019
$1.4M
NINDS NIH HHS R01 NS052669NINDS NIH HHS R01 NS097016NINDS NIH HHS R01 NS108750
6 · The paper itself

Abstract

Brief intracellular Ca(2+) transients initiate signaling routines that direct cellular activities. Consequently, activation of Ca(2+)-permeable neurotransmitter-gated channels can both depolarize and initiate remodeling of the postsynaptic cell. In particular, the Ca(2+) transient produced by NMDA receptors is essential to normal synaptic physiology, drives the development and plasticity of excitatory central synapses, and also mediates glutamate excitotoxicity. The amplitude and time course of the Ca(2+) signal depends on the receptor's conductance and gating kinetics; these properties are themselves influenced both directly and indirectly by fluctuations in the extracellular Ca(2+) concentration. Here, we used electrophysiology and kinetic modeling to delineate the direct effects of extracellular Ca(2+) on recombinant GluN1/GluN2A receptor conductance and gating. We report that, in addition to decreasing unitary conductance, Ca(2+) also decreased channel open probability primarily by lengthening closed-channel periods. Using one-channel current recordings, we derive a kinetic model for GluN1/GluN2A receptors in physiological Ca(2+) concentrations that accurately describes macroscopic channel behaviors. This model represents a practical instrument to probe the mechanisms that control the Ca(2+) transients produced by NMDA receptors during both normal and aberrant synaptic signaling.

Indexed as

Calcium SignalingIon Channel GatingAction PotentialsAnimalsCalciumHEK293 CellsHumansRatsReceptors, N-Methyl-D-AspartateCalciumReceptors, N-Methyl-D-Aspartate

Identifiers

PMID25348411
PMCPMC4210427
OpenAlexW2073709962

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.