Evidence map›Paper›PMID 16822976›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Altered balance of glutamatergic/GABAergic synaptic input and associated changes in dendrite morphology after BDNF expression in BDNF-deficient hippocampal neurons.

B Singh, C Henneberger, D Betances, M A Arevalo, A Rodríguez-Tébar, J C Meier, R Grantyn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. mGluR5 in hippocampal CA1 pyramidal neurons mediates stress-induced anxiety-like behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. The CaNeuropharmacology · 2022
    Article
  7. Article
  8. BDNF Expression in Cortical GABAergic Interneurons.International journal of molecular sciences · 2020
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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 3 institutions in 2 countries.

B SinghDevelopmental Physiology Group, Johannes Mueller Institute for Neurophysiology, University Medical School (Charité) of the Humboldt University, D-10117 Berlin, Germany.
C Henneberger
D Betances
M A Arevalo
A Rodríguez-Tébar
J C Meier
R Grantyn
Charité - Universitätsmedizin Berlin · DEHumboldt-Universität zu Berlin · DEInstituto Cajal · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cultured neurons from bdnf-/- mice display reduced densities of synaptic terminals, although in vivo these deficits are small or absent. Here we aimed at clarifying the local responses to postsynaptic brain-derived neurotrophic factor (BDNF). To this end, solitary enhanced green fluorescent protein (EGFP)-labeled hippocampal neurons from bdnf-/- mice were compared with bdnf-/- neurons after transfection with BDNF, bdnf-/- neurons after transient exposure to exogenous BDNF, and bdnf+/+ neurons in wild-type cultures. Synapse development was evaluated on the basis of presynaptic immunofluorescence and whole-cell patch-clamp recording of miniature postsynaptic currents. It was found that neurons expressing BDNF::EGFP for at least 16 h attracted a larger number of synaptic terminals than BDNF-deficient control neurons. Transfected BDNF formed clusters in the vicinity of glutamatergic terminals and produced a stronger upregulation of synaptic terminal numbers than high levels of ambient BDNF. Glutamatergic and GABAergic synapses reacted differently to postsynaptic BDNF: glutamatergic input increased, whereas GABAergic input decreased. BDNF::EGFP-expressing neurons also differed from BDNF-deficient neurons in their dendrite morphology: they exhibited weaker dendrite elongation and stronger dendrite initiation. The upregulation of glutamatergic synaptic input and the BDNF-induced downregulation of GABAergic synaptic terminal numbers by postsynaptic BDNF depended on tyrosine receptor kinase B activity, as deduced from the blocking effects of K252a. The suppression of dendrite elongation was also prevented by block of tyrosine receptor kinase B but required, in addition, glutamate receptor activity. Dendritic length decreased with the number of glutamatergic contacts. These results illuminate the role of BDNF as a retrograde synaptic regulator of synapse development and the dependence of dendrite elongation on glutamatergic input.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCells, CulturedDendritesEpidermal Growth FactorFemalegamma-Aminobutyric AcidGene ExpressionGlutamic AcidHippocampusMaleMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityNeuronsBrain-Derived Neurotrophic FactorEpidermal Growth Factorgamma-Aminobutyric AcidGlutamic AcidReceptor, Nerve Growth FactorReceptor, trkB

Identifiers

PMID16822976
PMCPMC6673958
OpenAlexW2001246997

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.