Evidence map›Paper›PMID 19706552›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Molecular mechanisms determining conserved properties of short-term synaptic depression revealed in NSF and SNAP-25 conditional mutants.

Fumiko Kawasaki, Richard W Ordway

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  10. Short-term synaptic depression is topographically distributed in the cochlear nucleus of the chicken.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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  14. Fast neurotransmitter release regulated by the endocytic scaffold intersectin.Proceedings of the National Academy of Sciences of the United States of America · 2013
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  15. Dance of the SNAREs: assembly and rearrangements detected with FRET at neuronal synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
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  16. Review
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  19. The DISABLED protein functions in CLATHRIN-mediated synaptic vesicle endocytosis and exoendocytic coupling at the active zone.Proceedings of the National Academy of Sciences of the United States of America · 2011
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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

2 authors at 1 institution in 1 country.

Fumiko KawasakiDepartment of Biology and Center for Molecular and Cellular Neuroscience, Pennsylvania State University, University Park, PA 16802, USA.
Richard W Ordway
Pennsylvania State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current models of synaptic vesicle trafficking implicate a core complex of proteins comprised of N-ethylmaleimide-sensitive factor (NSF), soluble NSF attachment proteins (SNAPs), and SNAREs in synaptic vesicle fusion and neurotransmitter release. Despite this progress, major challenges remain in establishing the in vivo functions of these proteins and their roles in determining the physiological properties of synapses. The present study employs glutamatergic adult neuromuscular synapses of Drosophila, which exhibit conserved properties of short-term synaptic plasticity with respect to mammalian glutamatergic synapses, to address these issues through genetic analysis. Our findings establish an in vivo role for SNAP-25 in synaptic vesicle priming, and support a zippering model of SNARE function in this process. Moreover, these studies define the contribution of SNAP-25-dependent vesicle priming to the detailed properties of short-term depression elicited by paired-pulse (PP) and train stimulation. In contrast, NSF is shown here not to be required for WT PP depression, but to be critical for maintaining neurotransmitter release during sustained stimulation. In keeping with this role, disruption of NSF function results in activity-dependent redistribution of the t-SNARE proteins, SYNTAXIN and SNAP-25, away from neurotransmitter release sites (active zones). These findings support a role for NSF in replenishing active zone t-SNAREs for subsequent vesicle priming, and provide new insight into the spatial organization of SNARE protein cycling during synaptic activity. Together, the results reported here establish in vivo contributions of SNAP-25 and NSF to synaptic vesicle trafficking and define molecular mechanisms determining conserved functional properties of short-term depression.

Indexed as

AnimalsDrosophila melanogasterDrosophila ProteinsElectrophysiologyEvoked PotentialsExcitatory Postsynaptic PotentialsImmunohistochemistryMutationN-Ethylmaleimide-Sensitive ProteinsNeuromuscular JunctionQa-SNARE ProteinsSNARE ProteinsSynapsesSynaptic VesiclesSynaptosomal-Associated Protein 25Time Factorscomt protein, DrosophilaDrosophila ProteinsN-Ethylmaleimide-Sensitive ProteinsQa-SNARE ProteinsSnap25 protein, DrosophilaSNARE ProteinsSynaptosomal-Associated Protein 25

Identifiers

PMID19706552
PMCPMC2732793
OpenAlexW2014194873

What OpenQuestion holds

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Registered trials

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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.