Evidence map›Paper›PMID 32943708›Full record

ArticleScientific reports2020

Traceable stimulus-dependent rapid molecular changes in dendritic spines in the brain.

Kazuya Kuboyama, Takafumi Inoue, Yuki Hashimotodani, Takuya Itoh, Tohsuke Suzuki, Aya Tetsuzawa, Yosuke Ohtsuka, Ryo Kinoshita, Ren Takara, Tohru Miyazawa and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

13 authors at 3 institutions in 1 country.

Kazuya KuboyamaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Takafumi InoueDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, 2-2 Wakamatsu-cho, Shinjuku, Tokyo, 162-8480, Japan.
Yuki HashimotodaniDepartment of Neurophysiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Takuya ItohDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Tohsuke SuzukiDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Aya TetsuzawaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Yosuke OhtsukaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Ryo KinoshitaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Ren TakaraDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Tohru MiyazawaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Pooja GusainLaboratory for Neural Circuit Systems, Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan.
Masanobu KanoDepartment of Neurophysiology, Graduate School of Medicine and International Research Center for Neurointelligence, The University of Tokyo Institutes for Advanced Study, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Maki K YamadaDepartment of Neuropharmacology, Kagawa School of Pharmaceutical Sciences and Institute of Neuroscience, Tokushima Bunri University, 1314-1 Shido, Sanuki, Kagawa, 769-2193, Japan. makiky-tky@umin.ac.jp.
Tokushima Bunri University · JPThe University of Tokyo · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic spines function as microcompartments that can modify the efficiency of their associated synapses. Here, we analyzed stimulus-dependent molecular changes in spines. The F-actin capping protein CapZ accumulates in parts of dendritic spines within regions where long-term potentiation has been induced. We produced a transgenic mouse line, AiCE-Tg, in which CapZ tagged with enhanced green fluorescence protein (EGFP-CapZ) is expressed. Twenty minutes after unilateral visual or somatosensory stimulation in AiCE-Tg mice, relative EGFP-CapZ signal intensification was seen in a subset of dendritic spines selectively in stimulated-side cortices; this right-left difference was abolished by NMDA receptor blockade. Immunolabeling of α-actinin, a PSD-95 binding protein that can recruit AMPA receptors, showed that the α-actinin signals colocalized more frequently in spines with the brightest EGFP-CapZ signals (top 100) than in spines with more typical EGFP-CapZ signal strength (top 1,000). This stimulus-dependent in vivo redistribution of EGFP-CapZ represents a novel molecular event with plasticity-like characteristics, and bright EGFP-CapZ in AiCE-Tg mice make high-CapZ spines traceable in vivo and ex vivo. This mouse line has the potential to be used to reveal sequential molecular events, including synaptic tagging, and to relate multiple types of plasticity in these spines, extending knowledge related to memory mechanisms.

Indexed as

ActininAnimalsBrainDendritic SpinesDisks Large Homolog 4 ProteinGreen Fluorescent ProteinsMiceMice, Inbred C57BLNeuronsReceptors, AMPAReceptors, N-Methyl-D-AspartateSignal TransductionSynapsesActininDisks Large Homolog 4 Proteinenhanced green fluorescent proteinGreen Fluorescent ProteinsReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID32943708
PMCPMC7499203
OpenAlexW3087609995

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.