Evidence map›Paper›PMID 25057210›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

SCAMP5 plays a critical role in synaptic vesicle endocytosis during high neuronal activity.

Haiyan Zhao, Yoonju Kim, Joohyun Park, Daehun Park, Sang-Eun Lee, Iree Chang, Sunghoe Chang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  8. Epilepsy-Related CDKL5 Deficiency Slows Synaptic Vesicle Endocytosis in Central Nerve Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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  19. nArgBP2 regulates excitatory synapse formation by controlling dendritic spine morphology.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

7 authors at 2 institutions in 3 countries.

Haiyan ZhaoDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center.
Yoonju KimDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center, Neuroscience Research Institute, Medical Research Center, and.
Joohyun ParkDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center, Neuroscience Research Institute, Medical Research Center, and.
Daehun ParkDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center.
Sang-Eun LeeDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center.
Iree ChangDepartment of Physiology and Biomedical Sciences.
Sunghoe ChangDepartment of Physiology and Biomedical Sciences, Biomembrane Plasticity Research Center, Neuroscience Research Institute, Medical Research Center, and Bio-Max Institute, Seoul National University College of Medicine, Seoul, South Korea 110-799 sunghoe@snu.ac.kr.
Institute of Biomedical Science · GBBioscience Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secretory carrier membrane protein 5 (SCAMP5), a recently identified candidate gene for autism, is brain specific and highly abundant in synaptic vesicles (SVs), but its function is currently unknown. Here, we found that knockdown (KD) of endogenous SCAMP5 by SCAMP5-specific shRNAs in cultured rat hippocampal neurons resulted in a reduction in total vesicle pool size as well as in recycling pool size, but the recycling/resting pool ratio was significantly increased. SCAMP5 KD slowed endocytosis after stimulation, but impaired it severely during strong stimulation. We also found that KD dramatically lowered the threshold of activity at which SV endocytosis became unable to compensate for the ongoing exocytosis occurring during a stimulus. Reintroducing shRNA-resistant SCAMP5 reversed these endocytic defects. Therefore, our results suggest that SCAMP5 functions during high neuronal activity when a heavy load is imposed on endocytosis. Our data also raise the possibility that the reduction in expression of SCAMP5 in autistic patients may be related to the synaptic dysfunction observed in autism.

Indexed as

AnimalsCarrier ProteinsEndocytosisFemaleGene Knockdown TechniquesHEK293 CellsHippocampusHumansMaleMembrane ProteinsNeuronsPrimary Cell CultureRatsRats, Sprague-DawleySynaptic VesiclesCarrier ProteinsMembrane ProteinsSCAMP5 protein, humanneuronal activityrecycling poolresting poolSCAMP5synaptic vesicle endocytosis

Identifiers

PMID25057210
PMCPMC6608302
OpenAlexW2073567531

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.