Evidence map›Paper›PMID 24740405›Full record

ArticlePloS one2014

Activity-dependent dendritic spine shrinkage and growth involve downregulation of cofilin via distinct mechanisms.

Barbara Calabrese, Jean-Michel Saffin, Shelley Halpain

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  7. MARCKS and PI(4,5)PMolecular biology of the cell · 2024
    Article
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  18. Review
  19. Synaptotoxicity in Alzheimer's Disease Involved a Dysregulation of Actin Cytoskeleton Dynamics through Cofilin 1 Phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  20. Actin blobs prefigure dendrite branching sites.The Journal of cell biology · 2018
    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

3 authors at 2 institutions in 1 country.

Barbara CalabreseDivision of Biological Sciences, and Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, United States of America.
Jean-Michel SaffinDivision of Biological Sciences, and Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, United States of America.
Shelley HalpainDivision of Biological Sciences, and Sanford Consortium for Regenerative Medicine, University of California San Diego, La Jolla, California, United States of America.
Sanford Consortium for Regenerative Medicine · USUniversity of California, San Diego · US

Funding

Mechanisms of Dendritic Spine StabilityR01MH087823 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HALPAIN, SHELLEY L · 2010 to 2014
$1.9M
REGULATION OF DENDRITIC SPINESR01NS037311 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI HALPAIN, SHELLEY L · 1999 to 2002
$960k
NIMH NIH HHS MH087823NIMH NIH HHS R01 MH087823NINDS NIH HHS NS37311NINDS NIH HHS R01 NS037311
6 · The paper itself

Abstract

A current model posits that cofilin-dependent actin severing negatively impacts dendritic spine volume. Studies suggested that increased cofilin activity underlies activity-dependent spine shrinkage, and that reduced cofilin activity induces activity-dependent spine growth. We suggest instead that both types of structural plasticity correlate with decreased cofilin activity. However, the mechanism of inhibition determines the outcome for spine morphology. RNAi in rat hippocampal cultures demonstrates that cofilin is essential for normal spine maintenance. Cofilin-F-actin binding and filament barbed-end production decrease during the early phase of activity-dependent spine shrinkage; cofilin concentration also decreases. Inhibition of the cathepsin B/L family of proteases prevents both cofilin loss and spine shrinkage. Conversely, during activity-dependent spine growth, LIM kinase stimulates cofilin phosphorylation, which activates phospholipase D-1 to promote actin polymerization. These results implicate novel molecular mechanisms and prompt a revision of the current model for how cofilin functions in activity-dependent structural plasticity.

Indexed as

Down-RegulationActinsAnimalsCells, CulturedCofilin 1Dendritic SpinesFemaleHippocampusImmunohistochemistryLim KinasesLong-Term PotentiationLong-Term Synaptic DepressionMicroscopy, ConfocalNeuronsN-MethylaspartatePhospholipase DActinsCofilin 1Lim KinasesN-MethylaspartatePhospholipase Dphospholipase D1Tacrolimus

Identifiers

PMID24740405
PMCPMC3989342
OpenAlexW2044844304

What Socratic 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 Socratic graph.