Evidence map›Paper›PMID 33770504›Full record

ArticleNeuron2021

An activity-dependent determinant of synapse elimination in the mammalian brain.

Masahiro Yasuda, Sivapratha Nagappan-Chettiar, Erin M Johnson-Venkatesh, Hisashi Umemori

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 77 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Masahiro YasudaDepartment of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Sivapratha Nagappan-ChettiarDepartment of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.
Erin M Johnson-VenkateshDepartment of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Hisashi UmemoriDepartment of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA. Electronic address: hisashi.umemori@childrens.harvard.edu.
Boston Children's Hospital · US

Funding

How do neurons in the brain decide to refine their synaptic connections in vivo?R01MH111647 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI Chinfei Chen, Hisashi Umemori · 2017 to 2026
$6.8M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
Investigating CD47-SIRPa as novel protective signals during CNS synaptic pruningR01NS092578 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI STEVENS, BETH ANN, UMEMORI, HISASHI · 2015 to 2019
$2.9M
Activity-Dependent Synapse Refinement in the Memory Circuit in vivoR01MH091429 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI UMEMORI, HISASHI · 2010 to 2014
$2.0M
NICHD NIH HHS U54 HD090255NIMH NIH HHS R01 MH091429NIMH NIH HHS R01 MH111647NINDS NIH HHS R01 NS092578
6 · The paper itself

Abstract

To establish functional neural circuits in the brain, synaptic connections are refined by neural activity during development, where active connections are maintained and inactive ones are eliminated. However, the molecular signals that regulate synapse refinement remain to be elucidated. When we inactivate a subset of neurons in the mouse cingulate cortex, their callosal connections are eliminated through activity-dependent competition. Using this system, we identify JAK2 tyrosine kinase as a key regulator of inactive synapse elimination. We show that JAK2 is necessary and sufficient for elimination of inactive connections; JAK2 is activated at inactive synapses in response to signals from other active synapses; STAT1, a substrate of JAK2, mediates inactive synapse elimination; JAK2 signaling is critical for physiological refinement of synapses during normal development; and JAK2 regulates synapse refinement in multiple brain regions. We propose that JAK2 is an activity-dependent switch that serves as a determinant of inactive synapse elimination.

Indexed as

AnimalsGyrus CinguliJanus Kinase 2MiceNeuronal PlasticityNeuronsSignal TransductionSTAT1 Transcription FactorSynapsesJanus Kinase 2STAT1 Transcription Factorcallosal synapsecompetitioninactive synapse eliminationJAK2 kinaseneural activityretinogeniculate synapseSTAT1synapse refinement

Identifiers

PMID33770504
PMCPMC8068677
OpenAlexW3138813354

What OpenQuestion holds

Textmetadata
LicenceTDM
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.