Evidence map›Paper›PMID 25426063›Full record

ArticleFrontiers in synaptic neuroscience2014

BDNF enhances spontaneous and activity-dependent neurotransmitter release at excitatory terminals but not at inhibitory terminals in hippocampal neurons.

Yo Shinoda, Saheeb Ahmed, Binu Ramachandran, Vinita Bharat, David Brockelt, Bekir Altas, Camin Dean

Open access · goldAbstract read
In one paragraph

Article in Frontiers in synaptic neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  13. Rb1, the Primary Active Ingredient inFrontiers in pharmacology · 2019
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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 1 institution in 2 countries.

Yo ShinodaTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany ; Department of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science Chiba, Japan.
Saheeb AhmedTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
Binu RamachandranTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
Vinita BharatTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
David BrockeltTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
Bekir AltasTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
Camin DeanTrans-synaptic Signaling Group, European Neuroscience Institute Goettingen, Germany.
European Neuroscience Institute Göttingen · DE

Funding

European Research Council 260916
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) is widely reported to enhance synaptic vesicle (SV) exocytosis and neurotransmitter release. But it is still unclear whether BDNF enhances SV recycling at excitatory terminals only, or at both excitatory and inhibitory terminals. In the present study, in a direct comparison using cultured rat hippocampal neurons, we demonstrate that BDNF enhances both spontaneous and activity-dependent neurotransmitter release from excitatory terminals, but not from inhibitory terminals. BDNF treatment for 5 min or 48 h increased both spontaneous and activity-induced anti-synaptotagmin1 (SYT1) antibody uptake at excitatory terminals marked with vGluT1. Conversely, BDNF treatment did not enhance spontaneous or activity-induced uptake of anti-SYT1 antibodies in inhibitory terminals marked with vGAT. Time-lapse imaging of FM1-43 dye destaining in excitatory and inhibitory terminals visualized by post-hoc immunostaining of vGluT1 and vGAT also showed the same result: The rate of spontaneous and activity-induced destaining was increased by BDNF at excitatory synapses, but not at inhibitory synapses. These data demonstrate that BDNF enhances SV exocytosis in excitatory but not inhibitory terminals. Moreover, BDNF enhanced evoked SV exocytosis, even if vesicles were loaded under spontaneous vesicle recycling conditions. Thus, BDNF enhances both spontaneous and activity-dependent neurotransmitter release on both short and long time-scales, by the same mechanism.

Indexed as

brain-derived neurotrophic factorexcitatory/inhibitoryexocytosishippocampal neuronsneurotransmitter release

Identifiers

PMID25426063
PMCPMC4226143
OpenAlexW2074417591

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.