Evidence map›Paper›PMID 34873044›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Sleep promotes the formation of dendritic filopodia and spines near learning-inactive existing spines.

Avital Adler, Cora Sau Wan Lai, Guang Yang, Erez Geron, Yang Bai, Wen-Biao Gan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  14. The role of calcium and CaMKII in sleep.Frontiers in systems neuroscience · 2022
    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

6 authors at 4 institutions in 3 countries.

Avital AdlerSkirball Institute, Department of Neuroscience and Physiology, Department of Anesthesiology, New York University School of Medicine, New York, NY 10016.
Cora Sau Wan LaiSchool of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China.ORCID 0000-0002-5721-4259
Guang YangDepartment of Anesthesiology, Columbia University Medical Center, New York, NY 10032.ORCID 0000-0002-5739-9126
Erez GeronSkirball Institute, Department of Neuroscience and Physiology, Department of Anesthesiology, New York University School of Medicine, New York, NY 10016.
Yang BaiSkirball Institute, Department of Neuroscience and Physiology, Department of Anesthesiology, New York University School of Medicine, New York, NY 10016.
Wen-Biao GanInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; wbgansky@gmail.com.
New York University · USPeking University · CNColumbia University Irving Medical Center · USUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Changes in synaptic connections are believed to underlie long-term memory storage. Previous studies have suggested that sleep is important for synapse formation after learning, but how sleep is involved in the process of synapse formation remains unclear. To address this question, we used transcranial two-photon microscopy to investigate the effect of postlearning sleep on the location of newly formed dendritic filopodia and spines of layer 5 pyramidal neurons in the primary motor cortex of adolescent mice. We found that newly formed filopodia and spines were partially clustered with existing spines along individual dendritic segments 24 h after motor training. Notably, posttraining sleep was critical for promoting the formation of dendritic filopodia and spines clustered with existing spines within 8 h. A fraction of these filopodia was converted into new spines and contributed to clustered spine formation 24 h after motor training. This sleep-dependent spine formation via filopodia was different from retraining-induced new spine formation, which emerged from dendritic shafts without prior presence of filopodia. Furthermore, sleep-dependent new filopodia and spines tended to be formed away from existing spines that were active at the time of motor training. Taken together, these findings reveal a role of postlearning sleep in regulating the number and location of new synapses via promoting filopodial formation.

Indexed as

AnimalsBacterial ProteinsCalciumDendritesFemaleLuminescent ProteinsMaleMiceMotor ActivityNeuronal PlasticityPseudopodiaPyramidal CellsRestraint, PhysicalSleepBacterial ProteinsCalciumLuminescent Proteinsyellow fluorescent protein, Bacteriaclusteringdendritic spinesfilopodiasleep

Identifiers

PMID34873044
PMCPMC8685900
OpenAlexW4200170201

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.