Evidence map›Paper›PMID 24394804›Full record

ArticleNature communications2014

A molecular brake controls the magnitude of long-term potentiation.

Yubin Wang, Guoqi Zhu, Victor Briz, Yu-Tien Hsu, Xiaoning Bi, Michel Baudry

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
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  9. T-type voltage-gated channels, NaCell communication and signaling : CCS · 2024
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  11. Review
  12. Article
  13. Calpain-2 Inhibitors as Therapy for Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  14. Polysaccharides fromOxidative medicine and cellular longevity · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Yubin Wang1] Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, California 91766, USA [2].
Guoqi Zhu1] Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, California 91766, USA [2].
Victor BrizGraduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, California 91766, USA.
Yu-Tien HsuStanford Institute of NeuroInnovation and Translational Neuroscience, Stanford University, Stanford, California 94305-5453, USA.
Xiaoning BiCollege of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, California 91766, USA.
Michel BaudryGraduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, California 91766, USA.
Western University of Health Sciences · US

Funding

The Spine Cytoskeleton and Memory DisordersP01NS045260 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 2003 to 2015
$14.4M
Simulation of learning: models and biological validationR01NS057128 · NINDS · WESTERN UNIVERSITY OF HEALTH SCIENCES · PI BAUDRY, MICHEL · 2009 to 2012
$2.2M
Ube3a and PKA regulation of SK2 channelsR15MH101703 · NIMH · WESTERN UNIVERSITY OF HEALTH SCIENCES · PI BI, XIAONING · 2014 to 2025
$1.7M
NIMH NIH HHS R15 MH101703NINDS NIH HHS P01 NS045260NINDS NIH HHS P01NS045260-01NINDS NIH HHS R01 NS057128NINDS NIH HHS R01NS057128
6 · The paper itself

Abstract

Overexpression of suprachiasmatic nucleus circadian oscillatory protein (SCOP), a negative ERK regulator, blocks long-term memory encoding. Inhibition of calpain-mediated SCOP degradation also prevents the formation of long-term memory, suggesting rapid SCOP breakdown is necessary for memory encoding. However, whether SCOP levels also control the magnitude of long-term synaptic plasticity is unknown. Here we show that following synaptic activity-induced SCOP degradation, SCOP is rapidly replaced via mTOR-mediated protein synthesis. We further show that early SCOP degradation is specifically catalysed by μ-calpain, whereas late SCOP resynthesis is mediated by m-calpain. We propose that μ-calpain promotes long-term potentiation induction by degrading SCOP and activating ERK, whereas m-calpain activation limits the magnitude of potentiation by terminating the ERK response via enhanced SCOP synthesis. This unique braking mechanism could account for the advantages of spaced versus massed training in the formation of long-term memory.

Indexed as

AnimalsCalpainHippocampusLong-Term PotentiationMaleMAP Kinase Signaling SystemMemory, Long-TermNeuronal PlasticityNuclear ProteinsPhosphoprotein PhosphatasesRatsRats, Sprague-DawleyCalpainm-calpainmu-calpainNuclear ProteinsPHLPP1 protein, ratPhosphoprotein Phosphatases

Identifiers

PMID24394804
PMCPMC3895372
OpenAlexW2031160794

What OpenQuestion holds

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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.