Evidence map›Paper›PMID 26041908›Full record

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

Autocrine action of BDNF on dendrite development of adult-born hippocampal neurons.

Liang Wang, Xingya Chang, Liang She, Duo Xu, Wei Huang, Mu-ming Poo

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 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 144 citations in OpenAlex.

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  14. Genetic deletion of zinc transporter ZnTFrontiers in molecular neuroscience · 2024
    Article
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12 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Liang WangInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031.
Xingya ChangInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031.
Liang SheInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031.
Duo XuInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031.
Wei HuangInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031.
Mu-ming PooInstitute of Neuroscience, State Key Laboratory of Neuroscience and CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Shanghai, China 200031 mpoo@ion.ac.cn.
University of Chinese Academy of Sciences · CNCenter for Excellence in Brain Science and Intelligence Technology · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendrite development of newborn granule cells (GCs) in the dentate gyrus of adult hippocampus is critical for their incorporation into existing hippocampal circuits, but the cellular mechanisms regulating their dendrite development remains largely unclear. In this study, we examined the function of brain-derived neurotrophic factor (BDNF), which is expressed in adult-born GCs, in regulating their dendrite morphogenesis. Using retrovirus-mediated gene transfection, we found that deletion and overexpression of BDNF in adult-born GCs resulted in the reduction and elevation of dendrite growth, respectively. This effect was mainly due to the autocrine rather than paracrine action of BDNF, because deletion of BDNF only in the newborn GCs resulted in dendrite abnormality of these neurons to a similar extent as that observed in conditional knockout (cKO) mice with BDNF deleted in the entire forebrain. Furthermore, selective expression of BDNF in adult-born GCs in BDNF cKO mice fully restored normal dendrite development. The BDNF autocrine action was also required for the development of normal density of spines and normal percentage of spines containing the postsynaptic marker PSD-95, suggesting autocrine BDNF regulation of synaptogenesis. Furthermore, increased dendrite growth of adult-born GCs caused by voluntary exercise was abolished by BDNF deletion specifically in these neurons and elevated dendrite growth due to BDNF overexpression in these neurons was prevented by reducing neuronal activity with coexpression of inward rectifier potassium channels, consistent with activity-dependent autocrine BDNF secretion. Therefore, BDNF expressed in adult-born GCs plays a critical role in dendrite development by acting as an autocrine factor.

Indexed as

ActinsAnalysis of VarianceAnimalsAnimals, NewbornBrain-Derived Neurotrophic FactorDendritesDisks Large Homolog 4 ProteinDoublecortin Domain ProteinsGuanylate KinasesHippocampusLuminescent ProteinsMembrane ProteinsMiceMice, Inbred C57BLMice, TransgenicMicrotubule-Associated ProteinsActinsBrain-Derived Neurotrophic FactorDisks Large Homolog 4 ProteinDlg4 protein, mouseDoublecortin Domain ProteinsGuanylate KinasesKirrel3 protein, mouseLuminescent ProteinsMembrane ProteinsMicrotubule-Associated ProteinsNes protein, mouseNestinNeuropeptidesautocrine actionBDNFdendrite development

Identifiers

PMID26041908
PMCPMC6605324
OpenAlexW1499836217

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.