Evidence map›Paper›PMID 10492006›Full record

ArticleLearning & memory (Cold Spring Harbor, N.Y.)

Signaling mechanisms mediating BDNF modulation of synaptic plasticity in the hippocampus.

W A Gottschalk, H Jiang, N Tartaglia, L Feng, A Figurov, B Lu

Open access · bronzeAbstract read
In one paragraph

Article in Learning & memory (Cold Spring Harbor, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
–field-weighted citation impact
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

70 citing papers in PubMed, 164 citations in OpenAlex.

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  14. mTOR inhibition impairs extinction memory reconsolidation.Learning & memory (Cold Spring Harbor, N.Y.) · 2021
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10 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.

W A GottschalkUnit on Synapse Development and Plasticity National Institute of Child Health and Development, National Institutes of Health, Bethesda, Maryland 20892-4480, USA.
H Jiang
N Tartaglia
L Feng
A Figurov
B Lu
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USHoward Hughes Medical Institute · USNational Institutes of Health · US

Funding

Molecular Mechanisms Of Synapse Development &PlasticityZ01HD000714 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LU, BAI · 1996 to 2008
$2.7M
6 · The paper itself

Abstract

Although recent studies indicate that brain-derived neurotrophic factor (BDNF) plays an important role in hippocampal synaptic plasticity, the underlying signaling mechanisms remain largely unknown. Here, we have characterized the signaling events that mediate the BDNF modulation of high-frequency synaptic transmission. Mitogen-associated protein kinase (MAPK), phosphotidylinositol-3 kinase (PI3K), and phospholipase C-gamma (PLC-gamma) are the three signaling pathways known to mediate neurotrophin signaling in other systems. In neonatal hippocampal slices, application of BDNF rapidly activated MAPK and PI3K but not PLC-gamma. BDNF greatly attenuated synaptic fatigue at CA1 synapses induced by a train of high-frequency, tetanic stimulation (HFS). Inhibition of the MAPK and PI3K, but not PLC-gamma, prevented the BDNF modulation of high-frequency synaptic transmission. Neurotrophin-3 (NT-3), a close relative of BDNF, did not activate MAPK or PI3K and had no effect on synaptic fatigue in the neonatal hippocampus. Neither forskolin, which activated MAPK but not PI3 kinase, nor ciliary neurotrophic factor (CNTF), which activated PI3K but not MAPK, affected HFS-induced synaptic fatigue. Treatment of the slices with forskolin together with CNTF still had no effect on synaptic fatigue. Thus, although the activation of MAPK and PI3K is required, the two together are not sufficient to mediate the BDNF effect. Inhibition of new protein synthesis by anisomycin or cycloheximide did not prevent the BDNF effect. These data suggest that BDNF modulation of high-frequency transmission is independent of protein synthesis but requires MAPK and PI3K and yet another signaling pathway to act together in the hippocampus.

Indexed as

AnimalsAnimals, NewbornBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein KinasesElectrophysiologyHippocampusIsoenzymesNerve Tissue ProteinsNeuronal PlasticityPhosphatidylinositol 3-KinasesPhospholipase C gammaRatsRats, Sprague-DawleySignal TransductionSynapsesType C PhospholipasesBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein KinasesIsoenzymesNerve Tissue ProteinsPhosphatidylinositol 3-KinasesPhospholipase C gammaType C Phospholipases

Identifiers

PMID10492006
PMCPMC311299
OpenAlexW1897264013

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.