Evidence map›Paper›PMID 26216953›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Activity-dependent BDNF release via endocytic pathways is regulated by synaptotagmin-6 and complexin.

Yu-Hui Wong, Chia-Ming Lee, Wenjun Xie, Bianxiao Cui, Mu-ming Poo

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
4.5field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Postsynaptic Complexin Mediates Constitutive Exocytosis of Nicotinic Acetylcholine Receptor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  7. Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025
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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

5 authors at 3 institutions in 2 countries.

Yu-Hui WongDivision of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720;
Chia-Ming LeeDivision of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720;
Wenjun XieDepartment of Chemistry, Stanford University, Stanford, CA 94305;
Bianxiao CuiDepartment of Chemistry, Stanford University, Stanford, CA 94305;
Mu-ming PooDivision of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720; Institute of Neuroscience, State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China mpoo@berkeley.edu.
Stanford University · USUniversity of California, Berkeley · USChinese Academy of Sciences · CN

Funding

Spike Timing-Dependent Plasticity of Neural CircuitsR01NS036999 · NINDS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI POO, MU-MING · 1998 to 2015
$3.8M
Engineering external forces for manipulating cargo transport in live neuronsDP2NS082125 · NINDS · STANFORD UNIVERSITY · PI CUI, BIANXIAO · 2012 to 2012
$2.4M
NINDS NIH HHS DP2 NS082125NINDS NIH HHS NS 036999NINDS NIH HHS R01 NS036999
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) is known to modulate synapse development and plasticity, but the source of synaptic BDNF and molecular mechanisms regulating BDNF release remain unclear. Using exogenous BDNF tagged with quantum dots (BDNF-QDs), we found that endocytosed BDNF-QDs were preferentially localized to postsynaptic sites in the dendrite of cultured hippocampal neurons. Repetitive neuronal spiking induced the release of BDNF-QDs at these sites, and this process required activation of glutamate receptors. Down-regulating complexin 1/2 (Cpx1/2) expression eliminated activity-induced BDNF-QD secretion, although the overall activity-independent secretion was elevated. Among eight synaptotagmin (Syt) isoforms examined, down-regulation of only Syt6 impaired activity-induced BDNF-QD secretion. In contrast, activity-induced release of endogenously synthesized BDNF did not depend on Syt6. Thus, neuronal activity could trigger the release of endosomal BDNF from postsynaptic dendrites in a Cpx- and Syt6-dependent manner, and endosomes containing BDNF may serve as a source of BDNF for activity-dependent synaptic modulation.

Indexed as

EndocytosisAdaptor Proteins, Vesicular TransportAnimalsAxonsBrain-Derived Neurotrophic FactorCalciumCell CompartmentationCells, CulturedDendritesDown-RegulationExocytosisGene Knockdown TechniquesGreen Fluorescent ProteinsHippocampusIntracellular SpaceMiceAdaptor Proteins, Vesicular TransportBrain-Derived Neurotrophic FactorCalciumcomplexin Ienhanced green fluorescent proteinGreen Fluorescent ProteinsNerve Tissue ProteinsReceptors, GlutamateSynaptotagminsBDNFcomplexinendocytosissecretionsynaptotagmin

Identifiers

PMID26216953
PMCPMC4538679
OpenAlexW1916496233

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.