Evidence map›Paper›PMID 15388780›Full record

ArticleThe Journal of physiology2004

Regulation of transmitter release by synapsin II in mouse motor terminals.

Dmitry Samigullin, Cynthia A Bill, William L Coleman, Maria Bykhovskaia

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.9field-weighted citation impact, top 35% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Electrophysiological analysis of synaptic transmission in Drosophila.Wiley interdisciplinary reviews. Developmental biology · 2017
    Review
  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. Synapsin Isoforms Regulating GABA Release from Hippocampal Interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  8. Defects in Neuromuscular Transmission May Underlie Motor Dysfunction in Spinal and Bulbar Muscular Atrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. 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
  13. Synapsin regulates activity-dependent outgrowth of synaptic boutons at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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. Alpha-synuclein loss in spinal muscular atrophy.Journal of molecular neuroscience : MN · 2011
    Article
  17. Article
  18. Article
  19. Article
  20. The role of synapsins in neuronal development.Cellular and molecular life sciences : CMLS · 2010
    Review
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 1 institution in 2 countries.

Dmitry SamigullinLehigh University, Department of Biological Sciences, Bethlehem, PA, USA.
Cynthia A Bill
William L Coleman
Maria Bykhovskaia
Lehigh University · 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 R01 MH61059
6 · The paper itself

Abstract

We investigated quantal release and ultrastructure in the neuromuscular junctions of synapsin II knockout (Syn II KO) mice. Synaptic responses were recorded focally from the diaphragm synapses during electrical stimulation of the phrenic nerve. We found that synapsin II affects transmitter release in a Ca(2+)-dependent manner. At reduced extracellular Ca(2+) (0.5 mM), Syn II KO mice demonstrated a significant increase in evoked and spontaneous quantal release, while at the physiological Ca(2+) concentration (2 mM), quantal release in Syn II KO synapses was unaffected. Protein kinase inhibitor H7 (100 microM) suppressed quantal release significantly stronger in Syn II KO synapses than in wild type (WT), indicating that Syn II KO synapses may compensate for the lack of synapsin II via a phosphorylation-dependent pathway. Electron microscopy analysis demonstrated that the lack of synapsin II results in an approximately 40% decrease in the density of synaptic vesicles in the reserve pool, while the number of vesicles docked to the presynaptic membrane remained unchanged. Synaptic depression in Syn II KO synapses was slightly increased, which is consistent with the depleted vesicle store in these synapses. At reduced Ca(2+) frequency facilitation of synchronous release was significantly increased in Syn II KO, while facilitation of asynchronous release was unaffected. Thus, at the reduced Ca(2+) concentration, synapsin II suppressed transmitter release and facilitation. These results demonstrate that synapsin II can regulate vesicle clustering, transmitter release, and facilitation.

Indexed as

1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAnimalsCalciumEnzyme InhibitorsMiceMice, Inbred StrainsMice, KnockoutMicroscopy, ElectronMotor NeuronsNeuromuscular JunctionPresynaptic TerminalsSynapsinsSynaptic TransmissionSynaptic Vesicles1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineCalciumEnzyme InhibitorsSynapsins

Identifiers

PMID15388780
PMCPMC1665329
OpenAlexW1536955969

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.