Evidence map›Paper›PMID 17412766›Full record

ArticleThe Journal of physiology2007

Astrocytic control of synaptic NMDA receptors.

C Justin Lee, Guido Mannaioni, Hongjie Yuan, Dong Ho Woo, Melissa B Gingrich, Stephen F Traynelis

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

125 citing papers in PubMed, 218 citations in OpenAlex.

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  12. Diversification of PAR signaling through receptor crosstalk.Cellular & molecular biology letters · 2022
    Review
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  18. Review
  19. Are glia targets for neuropathic orofacial pain therapy?Journal of the American Dental Association (1939) · 2021
    Article
  20. Article

65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

C Justin LeeCenter for Neural Science, Division of Life Sciences, Korea Institute of Science and Technology, Seoul, Korea.
Guido Mannaioni
Hongjie Yuan
Dong Ho Woo
Melissa B Gingrich
Stephen F Traynelis
Emory University · USKorea Institute of Science and Technology · KRUniversity of Florence · IT

Funding

NMDA RECEPTOR FUNCTION BY SERINE PROTEASE RECEPTORSR01NS039419 · NINDS · EMORY UNIVERSITY · PI TRAYNELIS, STEPHEN F. · 2000 to 2007
$2.6M
Modulation of NMDA receptors by serine proteases &PAR 1F32NS043875 · NINDS · EMORY UNIVERSITY · PI LEE, CHANGJOON J · 2002 to 2004
$98k
CONSEQUENCES OF NMDA RECEPTOR PROTEOLYSIS BY THROMBINF31MH011623 · NIMH · EMORY UNIVERSITY · PI BUTLER, MELISSA A · 1996 to 1997
–
NIMH NIH HHS F31 MH011623NIMH NIH HHS MH11623NINDS NIH HHS F32 NS043875NINDS NIH HHS NS39419NINDS NIH HHS NS43875NINDS NIH HHS R01 NS039419
6 · The paper itself

Abstract

Astrocytes express a wide range of G-protein coupled receptors that trigger release of intracellular Ca2+, including P2Y, bradykinin and protease activated receptors (PARs). By using the highly sensitive sniffer-patch technique, we demonstrate that the activation of P2Y receptors, bradykinin receptors and protease activated receptors all stimulate glutamate release from cultured or acutely dissociated astrocytes. Of these receptors, we have utilized PAR1 as a model system because of favourable pharmacological and molecular tools, its prominent expression in astrocytes and its high relevance to neuropathological processes. Astrocytic PAR1-mediated glutamate release in vitro is Ca2+ dependent and activates NMDA receptors on adjacent neurones in culture. Activation of astrocytic PAR1 in hippocampal slices induces an APV-sensitive inward current in CA1 neurones and causes APV-sensitive neuronal depolarization in CA1 neurones, consistent with release of glutamate from astrocytes. PAR1 activation enhances the NMDA receptor-mediated component of synaptic miniature EPSCs, evoked EPSCs and evoked EPSPs in a Mg2+-dependent manner, which may reflect spine head depolarization and consequent reduction of NMDA receptor Mg2+ block during subsequent synaptic currents. The release of glutamate from astrocytes following PAR1 activation may also lead to glutamate occupancy of some perisynaptic NMDA receptors, which pass current following relief of tonic Mg2+ block during synaptic depolarization. These results suggest that astrocytic G-protein coupled receptors that increase intracellular Ca2+ can tune synaptic NMDA receptor responses.

Indexed as

Calcium SignalingNeuronal PlasticityAnimalsAnimals, NewbornAstrocytesCalciumCells, CulturedCerebral CortexCoculture TechniquesExcitatory Postsynaptic PotentialsGlutamic AcidHippocampusHumansMagnesiumMiceMice, Inbred C57BLCalciumGlutamic AcidMagnesiumReceptor, PAR-1Receptors, N-Methyl-D-Aspartate

Identifiers

PMID17412766
PMCPMC2170820
OpenAlexW2164938885

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.