Evidence map›Paper›PMID 15240804›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons.

Tei-ichi Nishiki, George J Augustine

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

86 citing papers in PubMed, 168 citations in OpenAlex.

  1. Article
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  4. Synaptotagmin rings as high-sensitivity regulators of synaptic vesicle docking and fusion.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Deconstructing Synaptotagmin-1's Distinct Roles in Synaptic Vesicle Priming and Neurotransmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Molecular Evolution and Characterization of Fish Stathmin Genes.Animals : an open access journal from MDPI · 2020
    Article
  11. Article
  12. eLife · 2020
    Article
  13. Article
  14. Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020
    Article
  15. Article
  16. Synaptic vesicle protein 2: A multi-faceted regulator of secretion.Seminars in cell & developmental biology · 2019
    Review
  17. Article
  18. Nanomachinery Organizing Release at Neuronal and Ribbon Synapses.International journal of molecular sciences · 2019
    Review
  19. Article
  20. SNT-1 Functions as the CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article

26 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 2 institutions in 1 country.

Tei-ichi NishikiDepartment of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
George J Augustine
Duke Medical Center · USDuke University Hospital · US

Funding

ROLE OF CALCIUM IONS IN PRESYNAPTIC FUNCTIONR01NS021624 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AUGUSTINE, GEORGE J. · 1985 to 2009
$3.2M
Transmission at Synapsin-deficient SynapsesR01MH067044 · NIMH · DUKE UNIVERSITY · PI AUGUSTINE, GEORGE J. · 2003 to 2006
$1.2M
NIMH NIH HHS MH-67044NIMH NIH HHS R01 MH067044NINDS NIH HHS NS-21624NINDS NIH HHS R01 NS021624
6 · The paper itself

Abstract

We have asked whether loss of the Ca2+ sensor protein synaptotagmin I influences the total amount of neurotransmitter released after a presynaptic action potential. Hippocampal neurons from synaptotagmin I knock-out mice had a greatly reduced fast synchronous component of glutamate release, as reported previously. However, the amount of glutamate released during the slow asynchronous component increased in these knock-out neurons. As a result of these changes in the kinetics of release, there was no significant difference between wild-type and knock-out neurons in the total amount of transmitter released within 400 msec after a presynaptic stimulus. Fluorescence imaging experiments demonstrated that wild-type and knock-out neurons take up and release similar amounts of FM dye after depolarization, indicating normal amounts of synaptic vesicle trafficking in the knock-out neurons. These results indicate that synaptotagmin I knock-out neurons are fully capable of releasing neurotransmitter, with the increased slow component of release serving to compensate for loss of the fast component. Thus, synaptotagmin I synchronizes the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears to suppress the slower, asynchronous form of transmitter release.

Indexed as

AnimalsCalcium-Binding ProteinsCells, CulturedEndocytosisExcitatory Postsynaptic PotentialsExocytosisFluorescent DyesHippocampusMembrane GlycoproteinsMiceMice, KnockoutNerve Tissue ProteinsNeuronsNeurotransmitter AgentsPatch-Clamp TechniquesStimulation, ChemicalCalcium-Binding ProteinsFluorescent DyesMembrane GlycoproteinsNerve Tissue ProteinsNeurotransmitter AgentsSynaptotagmin ISynaptotagminsSyt1 protein, mouse

Identifiers

PMID15240804
PMCPMC6729667
OpenAlexW2165056042

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.