Evidence map›Paper›PMID 20920789›Full record

ArticleNeuron2010

Presynaptic activity and CaMKII modulate retrograde semaphorin signaling and synaptic refinement.

Robert A Carrillo, Douglas P Olsen, Kenneth S Yoon, Haig Keshishian

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Structural and Functional Synaptic Plasticity Induced by Convergent Synapse Loss in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  11. Article
  12. Synaptic Plasticity Induced by Differential Manipulation of Tonic and Phasic Motoneurons inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  13. Review
  14. Activity-Dependent Synaptic Plasticity inFrontiers in physiology · 2020
    Review
  15. Article
  16. Frontiers in genetics · 2019
    Article
  17. Plexin-Semaphorin Signaling Modifies Neuromuscular Defects in aFrontiers in molecular neuroscience · 2018
    Article
  18. Article
  19. Article
  20. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

4 authors at 1 institution in 1 country.

Robert A CarrilloPharmacology Department, Yale School of Medicine, New Haven, CT 06520, USA.
Douglas P Olsen
Kenneth S Yoon
Haig Keshishian
Yale University · US

Funding

CELLULAR AND MOLECULAR MECHANISMS OF SYNAPTOGENESISR01NS031651 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 1993 to 2013
$4.2M
Novel Molecular Tools for Transsynaptic Circuit AnalysisR21NS053807 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 2006 to 2007
$352k
NINDS NIH HHS 1R21NS053807NINDS NIH HHS 5R01NS031651NINDS NIH HHS R01 NS031651NINDS NIH HHS R21 NS053807
6 · The paper itself

Abstract

Establishing synaptic connections often involves the activity-dependent withdrawal of off-target contacts. We describe an in vivo role for temporally patterned electrical activity, voltage-gated calcium channels, and CaMKII in modulating the response of Drosophila motoneurons to the chemorepellent Sema-2a during synaptic refinement. Mutations affecting the Sema-2a ligand, the plexin B receptor (plexB), the voltage-gated Ca(v)2.1 calcium channel (cac), or the voltage-gated Na(v)1 sodium channel (mle(nap-ts);tipE) each result in ectopic neuromuscular contacts. Sema-2a interacts genetically with both of the channel mutations. The cac phenotype is enhanced by the Sema-2a mutation and is suppressed by either plexB overexpression or patterned, low-frequency (0.01 Hz) bouts of electrical activity in the embryo. The calcium-dependent suppression of ectopic contacts also depends on the downstream activation of CaMKII. These results indicate a role for patterned electrical activity and presynaptic calcium signaling, acting through CaMKII, in modulating a retrograde signal during the refinement of synaptic connections.

Indexed as

Neuromuscular JunctionAction PotentialsAnimalsAnimals, Genetically ModifiedCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, N-TypeCell Adhesion Molecules, NeuronalDrosophilaDrosophila ProteinsElectric StimulationEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGenetic TestingLarvaMotor NeuronsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, N-TypeCell Adhesion Molecules, NeuronalDrosophila Proteinsfasciclin IINerve Tissue ProteinsplexB protein, DrosophilaReceptors, Cell SurfaceSemaphorins

Identifiers

PMID20920789
PMCPMC2950831
OpenAlexW2028283773

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.