Evidence map›Paper›PMID 25609616›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

ATP binding to synaspsin IIa regulates usage and clustering of vesicles in terminals of hippocampal neurons.

Yoav Shulman, Alexandra Stavsky, Tatiana Fedorova, Dan Mikulincer, Merav Atias, Igal Radinsky, Joy Kahn, Inna Slutsky, Daniel Gitler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Fosgonimeton, a Novel Positive Modulator of the HGF/MET System, Promotes Neurotrophic and Procognitive Effects in Models of Dementia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Activity-Dependence of Synaptic Vesicle Dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. 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

9 authors at 3 institutions in 2 countries.

Yoav ShulmanDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel, and.
Alexandra StavskyDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel, and.
Tatiana FedorovaDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, and Sagol School of Neuroscience, Tel Aviv University, 69978 Tel Aviv, Israel.ORCID http://orcid.org/0000-0002-4740-7436
Dan MikulincerDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and.
Merav AtiasDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and.
Igal RadinskyDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and.
Joy KahnDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and.
Inna SlutskyDepartment of Physiology and Pharmacology, Sackler Faculty of Medicine, and Sagol School of Neuroscience, Tel Aviv University, 69978 Tel Aviv, Israel.
Daniel GitlerDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel, and gitler@bgu.ac.il.ORCID http://orcid.org/0000-0001-9544-3610
Faculty of Public Health · GBBen-Gurion University of the Negev · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic transmission is expensive in terms of its energy demands and was recently shown to decrease the ATP concentration within presynaptic terminals transiently, an observation that we confirm. We hypothesized that, in addition to being an energy source, ATP may modulate the synapsins directly. Synapsins are abundant neuronal proteins that associate with the surface of synaptic vesicles and possess a well defined ATP-binding site of undetermined function. To examine our hypothesis, we produced a mutation (K270Q) in synapsin IIa that prevents ATP binding and reintroduced the mutant into cultured mouse hippocampal neurons devoid of all synapsins. Remarkably, staining for synaptic vesicle markers was enhanced in these neurons compared with neurons expressing wild-type synapsin IIa, suggesting overly efficient clustering of vesicles. In contrast, the mutation completely disrupted the capability of synapsin IIa to slow synaptic depression during sustained 10 Hz stimulation, indicating that it interfered with synapsin-dependent vesicle recruitment. Finally, we found that the K270Q mutation attenuated the phosphorylation of synapsin IIa on a distant PKA/CaMKI consensus site known to be essential for vesicle recruitment. We conclude that ATP binding to synapsin IIa plays a key role in modulating its function and in defining its contribution to hippocampal short-term synaptic plasticity.

Indexed as

Adenosine TriphosphateAnimalsCells, CulturedHippocampusMiceMice, KnockoutNeuronsPresynaptic TerminalsSynapsinsSynaptic TransmissionSynaptic VesiclesAdenosine TriphosphateSynapsinsATPphosphorylationshort-term plasticitysynapsinsynaptic vesiclevesicle pools

Identifiers

PMID25609616
PMCPMC6605539
OpenAlexW2095325838

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.