Evidence map›Paper›PMID 24431436›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Neurofibromin is the major ras inactivator in dendritic spines.

Ana F Oliveira, Ryohei Yasuda

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Endogenous PTEN-Induced Kinase 1 Regulates Dendritic Architecture and Spinogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  16. Review
  17. Article
  18. mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022
    Review
  19. Blockade of Serotonin 5-HTInternational journal of molecular sciences · 2021
    Article
  20. Review
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 2 institutions in 2 countries.

Ana F OliveiraDepartment of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, Howard Hughes Medical Institute, Duke University Medical Center, Durham, North Carolina 27710, Max-Planck Florida Institute for Neuroscience, Jupiter, Florida 33458, and Doctoral Program in Biomedicine and Experimental Biology, Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.
Ryohei Yasuda
Duke Medical Center · USDuke University Hospital · US

Funding

Mechanisms of Ras Signaling in Single SynapsesR01MH080047 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2007 to 2023
$6.8M
Imaging signal transduction in single dendritic spinesR01NS068410 · NINDS · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2009 to 2013
$2.0M
Large Scale Development of Sensors for Imaging Small GTPase Signals in SynapsesR01MH095090 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2011 to 2014
$1.7M
Howard Hughes Medical InstituteNIMH NIH HHS R01 MH080047NIMH NIH HHS R01 MH095090NINDS NIH HHS R01 NS068410
6 · The paper itself

Abstract

In dendritic spines, Ras plays a critical role in synaptic plasticity but its regulation mechanism is not fully understood. Here, using a fluorescence resonance energy transfer/fluorescence lifetime imaging microscopy-based Ras imaging technique in combination with 2-photon glutamate uncaging, we show that neurofibromin, in which loss-of-function mutations cause Neurofibromatosis Type 1 (NF1), contributes to the majority (∼90%) of Ras inactivation in dendritic spines of pyramidal neurons in the CA1 region of the rat hippocampus. Loss of neurofibromin causes sustained Ras activation in spines, which leads to impairment of spine structural plasticity and loss of spines in an activity-dependent manner. Therefore, deregulation of postsynaptic Ras signaling may explain, at least in part, learning disabilities associated with NF1.

Indexed as

AnimalsCells, CulturedDendritic SpinesExcitatory Postsynaptic PotentialsFemaleGenes, rasHippocampusLong-Term PotentiationMaleNeurofibromin 1Organ Culture TechniquesRatsRats, Sprague-DawleyNeurofibromin 1hippocampusLTPNF1NMDA receptorratssmall GTPasesynaptic plasticity

Identifiers

PMID24431436
PMCPMC3891958
OpenAlexW2005843414

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.