Evidence map›Paper›PMID 19858225›Full record

ArticleThe Journal of physiology2009

Synaptically induced sodium signals in hippocampal astrocytes in situ.

Julia Langer, Christine R Rose

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

75 citing papers in PubMed, 150 citations in OpenAlex.

  1. Overactive EAAT1 ClActa neuropathologica communications · 2026
    Article
  2. Review
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  4. Article
  5. Functional CaScientific reports · 2026
    Article
  6. Spatiotemporal Dynamics of Lateral NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  7. Prototype Magnetic Deflector System for Light Element Particle Induced X-Ray Emission Analysis.Nuclear instruments & methods in physics research. Section B, Beam interactions with materials and atoms · 2025
    Article
  8. Review
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  10. Spatio-temporal dynamics of lateral NabioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022
    Review
  18. Changes in Astroglial KInternational journal of molecular sciences · 2022
    Article
  19. Review
  20. On the origin of ultraslow spontaneous NaJournal of neurophysiology · 2021
    Article

15 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

2 authors at 1 institution in 1 country.

Julia LangerInstitute for Neurobiology, Heinrich-Heine-University Duesseldorf, Universitaetsstrasse 1, 26.02.00, 40225 Duesseldorf, Germany.
Christine R Rose
Heinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes are in close contact to excitatory synapses and express transporters which mediate the sodium-dependent uptake of glutamate. In cultured astrocytes, selective activation of glutamate transport results in sodium elevations which stimulate Na(+)/K(+)-ATPase and glucose uptake, indicating that synaptic release of glutamate might couple excitatory neuronal activity to glial sodium homeostasis and metabolism. Here, we analysed intracellular sodium transients evoked by synaptic stimulation in acute mouse hippocampal slices using quantitative sodium imaging with the sodium-sensitive fluorescent indicator dye SBFI (sodium-binding benzofuran isophthalate). We found that short bursts of Schaffer collateral stimulation evoke sodium transients in the millimolar range in both CA1 pyramidal neurons and in SR101-positive astrocytes of the stratum radiatum. At low stimulation intensities, glial sodium transients were confined to one to two primary branches and adjacent fine processes and only weakly invaded the soma. Increasing the number of activated afferent fibres by increasing the stimulation intensity elicited global sodium transients detectable in the processes as well as the somata of astrocytes. Pharmacological analysis revealed that neuronal sodium signals were mainly attributable to sodium influx through ionotropic glutamate receptors. Activation of ionotropic receptors also contributed to glial sodium transients, while TBOA-sensitive glutamate transport was the major pathway responsible for sodium influx into astrocytes. Our results thus establish that glutamatergic synaptic transmission in the hippocampus results in sodium transients in astrocytes that are mainly mediated by activation of glutamate transport. They support the proposed link between excitatory synaptic activity, glutamate uptake and sodium signals in astrocytes of the hippocampus.

Indexed as

AnimalsAstrocytesCells, CulturedGlutamic AcidHippocampusMiceMice, Inbred BALB CSodiumSynaptic TransmissionGlutamic AcidSodium

Identifiers

PMID19858225
PMCPMC2808545
OpenAlexW1594253922

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.