Evidence map›Paper›PMID 18579739›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Two forms of astrocyte calcium excitability have distinct effects on NMDA receptor-mediated slow inward currents in pyramidal neurons.

Eiji Shigetomi, David N Bowser, Michael V Sofroniew, Baljit S Khakh

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed
7.4field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 255 citations in OpenAlex.

  1. Article
  2. Article
  3. Ultrastructural Characteristics of the Juvenile Chum Salmon (International journal of molecular sciences · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Disease-relevant upregulation of P2YNature communications · 2024
    Article
  9. Article
  10. Astrocytes as Drivers and Disruptors of Behavior: New Advances in Basic Mechanisms and Therapeutic Targeting.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
  11. Article
  12. Dysregulation of astrocytic CaActa neuropathologica · 2023
    Article
  13. Review
  14. Calcium signaling in astrocytes and gliotransmitter release.Frontiers in synaptic neuroscience · 2023
    Review
  15. Astrocytic modulation of neuronal signalling.Frontiers in network physiology · 2023
    Review
  16. Review
  17. CaNature communications · 2022
    Article
  18. Article
  19. Article
  20. Review

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

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

4 authors at 3 institutions in 2 countries.

Eiji ShigetomiDepartments of Physiology and Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, California 90095-1751, USA.
David N Bowser
Michael V Sofroniew
Baljit S Khakh
Medical Research Council · GBMRC Laboratory of Molecular Biology · GBUniversity of California, Los Angeles · US

Funding

Functions of astrocyte calcium signaling in the striatumR01NS060677 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KHAKH, BALJIT · 2008 to 2018
$4.3M
Medical Research CouncilNINDS NIH HHS R01 NS060677
6 · The paper itself

Abstract

Astrocytes display excitability in the form of intracellular calcium concentration ([Ca(2+)](i)) increases, but the signaling impact of these for neurons remains debated and controversial. A key unresolved issue is whether astrocyte [Ca(2+)](i) elevations impact neurons or not. Here we report that in the CA1 region of the hippocampus, agonists of native P2Y(1) and PAR-1 receptors, which are preferentially expressed in astrocytes, equally elevated [Ca(2+)](i) levels without affecting the passive membrane properties of pyramidal neurons. However, under conditions chosen to isolate NMDA receptor responses, we found that activation of PAR-1 receptors led to the appearance of NMDA receptor-mediated slow inward currents (SICs) in pyramidal neurons. In stark contrast, activation of P2Y(1) receptors was ineffective in this regard. The PAR-1 receptor-mediated increased SICs were abolished by several strategies that selectively impaired astrocyte [Ca(2+)](i) excitability and function. Our studies therefore indicate that evoked astrocyte [Ca(2+)](i) transients are not a binary signal for interactions with neurons, and that astrocytes result in neuronal NMDA receptor-mediated SICs only when appropriately excited. The data thus provide a basis to rationalize recent contradictory data on astrocyte-neuron interactions.

Indexed as

AnimalsAstrocytesCalciumCalcium SignalingCell CommunicationGlutamic AcidHippocampusMembrane PotentialsMiceMice, Inbred C57BLMice, TransgenicOrgan Culture TechniquesPurinergic P2 Receptor AgonistsPyramidal CellsReceptor, PAR-1Receptors, N-Methyl-D-AspartateCalciumGlutamic AcidP2ry1 protein, mousePurinergic P2 Receptor AgonistsReceptor, PAR-1Receptors, N-Methyl-D-AspartateReceptors, Purinergic P2Receptors, Purinergic P2Y1

Identifiers

PMID18579739
PMCPMC2866443
OpenAlexW2006395355

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.