Evidence map›Paper›PMID 18669537›Full record

ArticleThe Journal of physiology2008

Synapsin II and calcium regulate vesicle docking and the cross-talk between vesicle pools at the mouse motor terminals.

William L Coleman, Cynthia A Bill, Fatma Simsek-Duran, György Lonart, Dmitry Samigullin, Maria Bykhovskaia

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. Article
  6. Synapsin II Regulation of GABAergic Synaptic Transmission Is Dependent on Interneuron Subtype.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  7. Article
  8. ATP binding to synaspsin IIa regulates usage and clustering of vesicles in terminals of hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  9. Article
  10. Article
  11. Synapsin II and Rab3a cooperate in the regulation of epileptic and synaptic activity in the CA1 region of the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Synapsin selectively controls the mobility of resting pool vesicles at hippocampal terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  16. A new kinetic framework for synaptic vesicle trafficking tested in synapsin knock-outs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  17. Article
  18. Article
  19. Article
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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

6 authors at 2 institutions in 1 country.

William L ColemanDepartment of Biological Sciences, Lehigh University, Bethlehem, PA 18015, USA. mabv@lehigh.edu
Cynthia A Bill
Fatma Simsek-Duran
György Lonart
Dmitry Samigullin
Maria Bykhovskaia
Lehigh University · USEastern Virginia Medical School · US

Funding

QUANTITATIVE STUDY OF PRESYNAPTIC FACILITATIONR01MH061059 · NIMH · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BYKHOVSKAIA, MARIA · 2000 to 2010
$2.2M
NIMH NIH HHS R01 MH061059NIMH NIH HHS R01MH61059
6 · The paper itself

Abstract

The synapsins, an abundant and highly conserved family of proteins that associate with synaptic vesicles, have been implicated in regulating the synaptic vesicle cycle. However, it has not been determined whether synapsin directly regulates the number of docked vesicles. Here we document that reducing Ca(2+) concentration [Ca(2+)](o) in the extracellular medium from 2 to 0.5 mm led to an approximately 40% decrease in both docked and undocked synaptic vesicles in wild-type nerve terminals of the mouse diaphragm. The same treatment reduced the number of undocked vesicles in nerve terminals derived from synapsin II gene deleted animals, but surprisingly it did not decrease vesicle docking, indicating that synapsin II inhibits docking of synaptic vesicles at reduced [Ca(2+)](o). In accordance with the morphological findings, at reduced [Ca(2+)](o) synapsin II (-) terminals had a higher rate of quantal neurotransmitter release. Microinjection of a recombinant synapsin II protein into synapsin II (-) terminals reduced vesicular docking and inhibited quantal release, indicating a direct and selective synapsin II effect for regulating vesicle docking and, in turn, quantal release. To understand why [Ca(2+)](o) has a prominent effect on synapsin function, we investigated the effect of [Ca(2+)](o) on the distribution of synaptic vesicles and on the concentration of intraterminal Ca(2+). We found that reduced [Ca(2+)](o) conditions produce a decrease in intracellular Ca(2+) and overall vesicle depletion. To explore why at these conditions the role of synapsin II in vesicle docking becomes more prominent, we developed a quantitative model of the vesicle cycle, with a two step synapsin action in stabilizing the vesicle store and regulating vesicle docking. The results of the modelling were in a good agreement with the observed dependence of vesicle distribution on synapsin II and calcium deficiency.

Indexed as

AnimalsCalciumDiaphragmMiceMice, KnockoutModels, BiologicalNeuromuscular JunctionNeurotransmitter AgentsReceptor Cross-TalkSynapsinsSynaptic VesiclesCalciumNeurotransmitter AgentsSynapsins

Identifiers

PMID18669537
PMCPMC2614040
OpenAlexW1603483721

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.