Evidence map›Paper›PMID 11404410›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

BDNF enhances quantal neurotransmitter release and increases the number of docked vesicles at the active zones of hippocampal excitatory synapses.

W J Tyler, L D Pozzo-Miller

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 1 pooled it
7.1field-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

242 citing papers in PubMed, 1 synthesis or guideline pooled it, 512 citations in OpenAlex.

  1. Pooled it
  2. Review of in vitro approaches for assessing the toxicity of chemical stressors across diverse physiological systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026
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  17. Brain-derived neurotrophic factor scales presynaptic calcium transients to modulate excitatory neurotransmission.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  19. Article
  20. Review

182 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

2 authors at 1 institution in 1 country.

W J TylerDepartment of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0021, USA.
L D Pozzo-Miller
University of Alabama at Birmingham · US

Funding

White mater neurons &nitric oxide in neonatal neocortexP01HD038760 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FRIEDLANDER, MICHAEL J · 2000 to 2004
$3.9M
ACTIONS OF BDNF ON CA2+ SIGNALS IN HIPPOCAMPAL NEURONSR01NS040593 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2000 to 2010
$2.8M
NICHD NIH HHS P01 HD038760NICHD NIH HHS P01-HD38760NINDS NIH HHS R01 NS040593NINDS NIH HHS R01-NS40593-01
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) is emerging as a key mediator of activity-dependent modifications of synaptic strength in the CNS. We investigated the hypothesis that BDNF enhances quantal neurotransmitter release by modulating the distribution of synaptic vesicles within presynaptic terminals using organotypic slice cultures of postnatal rat hippocampus. BDNF specifically increased the number of docked vesicles at the active zone of excitatory synapses on CA1 dendritic spines, with only a small increase in active zone size. In agreement with the hypothesis that an increased docked vesicle density enhances quantal neurotransmitter release, BDNF increased the frequency, but not the amplitude, of AMPA receptor-mediated miniature EPSCs (mEPSCs) recorded from CA1 pyramidal neurons in hippocampal slices. Synapse number, independently estimated from dendritic spine density and electron microscopy measurements, was also increased after BDNF treatment, indicating that the actions of BNDF on mEPSC frequency can be partially attributed to an increased synaptic density. Our results further suggest that all these actions were mediated via tyrosine kinase B (TrkB) receptor activation, established by inhibition of plasma membrane tyrosine kinases with K-252a. These results provide additional evidence of a fundamental role of the BDNF-TrkB signaling cascade in synaptic transmission, as well as in cellular models of hippocampus-dependent learning and memory.

Indexed as

alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsBrain-Derived Neurotrophic FactorDendritesEnzyme InhibitorsExcitatory Postsynaptic PotentialsHippocampusIn Vitro TechniquesNeurotransmitter AgentsPresynaptic TerminalsPyramidal CellsRatsRats, Sprague-DawleyReceptors, AMPAReceptor, trkBSignal Transductionalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidBrain-Derived Neurotrophic FactorEnzyme InhibitorsNeurotransmitter AgentsReceptors, AMPAReceptor, trkB

Identifiers

PMID11404410
PMCPMC2806848
OpenAlexW2146493911

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.