Evidence map›Paper›PMID 40986440›Full record

ArticleeLife2025

Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.

Jie Wang, Jun Nishiyama, Paula Parra-Bueno, Elwy Okaz, Goksu Oz, Xiaodan Liu, Tetsuya Watabe, Irena Suponitsky-Kroyter, Timothy E McGraw, Erzsebet M Szatmari and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Jie WangDepartment of Neurobiology, Duke University School of Medicine, Durham, United States.ORCID https://orcid.org/0000-0002-3530-5029
Jun NishiyamaNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.ORCID https://orcid.org/0000-0002-3627-8114
Paula Parra-BuenoNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Elwy OkazNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Goksu OzNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Xiaodan LiuNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Tetsuya WatabeNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Irena Suponitsky-KroyterNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.
Timothy E McGrawWeill Cornell Medicine Graduate School of Medical Sciences, New York, United States.ORCID https://orcid.org/0000-0001-9748-263X
Erzsebet M SzatmariNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.ORCID https://orcid.org/0000-0002-2914-6148
Ryohei YasudaNeuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.ORCID https://orcid.org/0000-0001-6263-9297

Funding

Mechanisms of Ras Signaling in Single SynapsesR01MH080047 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2007 to 2023
$6.8M
Deciphering Biochemical Networks in Single Dendritic SpinesDP1NS096787 · NINDS · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2015 to 2019
$4.8M
Validation of Fibroblast-Derived PI16 as a Novel Target for pain TreatmentR01NS116704 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SHEPHERD, ANDREW JOHN · 2020 to 2024
$3.6M
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
Japan Society for the Promotion of Science Overseas Research Fellowship 667NIMH NIH HHS R01 MH080047NIMH NIH HHS R01MH080047NIMH NIH HHS R01 MH095090NIMH NIH HHS R01MH095090NINDS NIH HHS DP1 NS096787NINDS NIH HHS DP1NS096787NINDS NIH HHS R01 NS116704NINDS NIH HHS R35NS116704
6 · The paper itself

Abstract

Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ~5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP, and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.

Indexed as

Dendritic SpinesLong-Term Potentiationrab GTP-Binding ProteinsReceptors, AMPAAnimalsHippocampusMiceProtein TransportRatsrab GTP-Binding ProteinsReceptors, AMPAdendritic spinesFLIMFRETGTPasemouseneuroscienceplasticityrabrat

Identifiers

PMID40986440
PMCPMC12456950

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.