Evidence map›Paper›PMID 15197251›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Synaptotagmin IV regulates glial glutamate release.

Qi Zhang, Mitsunori Fukuda, Elisabeth Van Bockstaele, Olivier Pascual, Philip G Haydon

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
5.9field-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

90 citing papers in PubMed, 205 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Cells and Molecules Underpinning Cannabis-Related Variations in Cortical Thickness during Adolescence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Exocytosis in Astrocytes.Biomolecules · 2021
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

30 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

5 authors at 2 institutions in 2 countries.

Qi ZhangDepartment of Neuroscience, Room 215, Stemmler Hall, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Mitsunori Fukuda
Elisabeth Van Bockstaele
Olivier Pascual
Philip G Haydon
University of Pennsylvania · USThomas Jefferson University · US

Funding

Reciprocal Signaling between Synapses and AstrocytesR01NS043142 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HAYDON, PHILIP G · 2001 to 2010
$4.0M
Astrocyte-Neuron SignalingR37NS037585 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HAYDON, PHILIP G · 2002 to 2008
$2.7M
NINDS NIH HHS R01 NS043142NINDS NIH HHS R01 NS43142NINDS NIH HHS R37 NS037585NINDS NIH HHS R37 NS37585
6 · The paper itself

Abstract

Calcium-binding synaptotagmins (Syts) are membrane proteins that are conserved from nematode to human. Fifteen Syts (Syts I-XV) have been identified in mammalian species. Syt I has been well studied and is a candidate for the Ca(2+)-sensor that triggers evoked exocytosis underlying fast synaptic transmission. Whereas the functions of the other Syts are unclear, Syt IV is of particular interest because it is rapidly up-regulated after chronic depolarization or seizures, and because null mutations exhibit deficits in fine motor coordination and hippocampus-dependent memory. Screening Syts I-XIII, which are enriched in brain, we find that Syt IV is located in processes of astroglia in situ. Reduction of Syt IV in astrocytes by RNA interference decreases Ca(2+)-dependent glutamate release, a gliotransmission pathway that regulates synaptic transmission. Mutants of the C2B domain, the only putative Ca(2+)-binding domain in Syt IV, act in a dominant-negative fashion over Ca(2+)-regulated glial glutamate release, but not gliotransmission induced by changes in osmolarity. Because we find that Syt IV is expressed predominantly by astrocytes and is not in the presynaptic terminals of the hippocampus, and because Syt IV knockout mice exhibit hippocampal-based memory deficits, our data raise the intriguing possibility that Syt IV-mediated gliotransmission contributes to hippocampal-based memory.

Indexed as

Calcium-Binding ProteinsAnimalsAnimals, NewbornAstrocytesCalciumCell Culture TechniquesCerebral CortexGlutamic AcidHippocampusMembrane GlycoproteinsMiceMice, KnockoutMice, TransgenicMutagenesis, Site-DirectedNerve Tissue ProteinsNeurogliaCalciumCalcium-Binding ProteinsGlutamic AcidMembrane GlycoproteinsNerve Tissue ProteinsReceptors, Cell SurfaceRecombinant ProteinsRNA, Small InterferingSynaptotagminsSyt4 protein, mouse

Identifiers

PMID15197251
PMCPMC438995
OpenAlexW2117530806

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.