Evidence map›Paper›PMID 28626015›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Reciprocal Interaction of Dendrite Geometry and Nuclear Calcium-VEGFD Signaling Gates Memory Consolidation and Extinction.

Thekla J Hemstedt, C Peter Bengtson, Omar Ramírez, Ana M M Oliveira, Hilmar Bading

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  5. Dysregulation ofLearning & memory (Cold Spring Harbor, N.Y.) · 2022
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  8. Soluble CD163 Changes Indicate Monocyte Association With Cognitive Deficits in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
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  11. Nasally delivered VEGFD mimetics mitigate stroke-induced dendrite loss and brain damage.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

5 authors at 1 institution in 2 countries.

Thekla J HemstedtDepartment of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany.ORCID 0000-0002-1765-9712
C Peter BengtsonDepartment of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany.ORCID 0000-0002-8245-3323
Omar RamírezDepartment of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany.ORCID 0000-0002-9326-2290
Ana M M OliveiraDepartment of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany.ORCID 0000-0002-2729-9036
Hilmar BadingDepartment of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University, 69120 Heidelberg, Germany bading@nbio.uni-heidelberg.de.ORCID 0000-0003-0258-4348
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear calcium is an important signaling end point in synaptic excitation-transcription coupling that is critical for long-term neuroadaptations. Here, we show that nuclear calcium acting via a target gene, VEGFD, is required for hippocampus-dependent fear memory consolidation and extinction in mice. Nuclear calcium-VEGFD signaling upholds the structural integrity and complexity of the dendritic arbor of CA1 neurons that renders those cells permissive for the efficient generation of synaptic input-evoked nuclear calcium transients driving the expression of plasticity-related genes. Therefore, the gating of memory functions rests on the reciprocally reinforcing maintenance of an intact dendrite geometry and a functional synapse-to-nucleus communication axis. In psychiatric and neurodegenerative disorders, therapeutic application of VEGFD may help to stabilize dendritic structures and network connectivity, which may prevent cognitive decline and could boost the efficacy of extinction-based exposure therapies.

Indexed as

AnimalsCalciumCalcium SignalingCell NucleusDendritesExtinction, PsychologicalMaleMemory ConsolidationMental RecallMiceMice, Inbred C57BLNeuronal PlasticityRetention, PsychologySignal TransductionVascular Endothelial Growth Factor DCalciumVascular Endothelial Growth Factor Dcalcium signalingdendrite morphologygene expressionmemory functionnuclear calciumVEGFD

Identifiers

PMID28626015
PMCPMC6705723
OpenAlexW2624736346

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.