Evidence map›Paper›PMID 27281494›Full record

ArticleDevelopmental neurobiology2017

Cyclic nucleotide signaling is required during synaptic refinement at the Drosophila neuromuscular junction.

Fernando Vonhoff, Haig Keshishian

Open access · greenAbstract read
In one paragraph

Article in Developmental neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. cAMP/PKA signaling regulates TDP-43 aggregation and mislocalization.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. 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
  7. Review
  8. Activity-Dependent Synaptic Plasticity inFrontiers in physiology · 2020
    Review
  9. Article
  10. Dissecting Motor Neuron Disease WithFrontiers in neuroscience · 2019
    Review
  11. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  12. Review
  13. Activity-Dependent Synaptic Refinement: New Insights fromFrontiers in systems neuroscience · 2017
    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

2 authors at 1 institution in 2 countries.

Fernando VonhoffMolecular, Cellular, and Developmental Biology Department, Yale University, POB 208103, New Haven, Connecticut, 06520.ORCID 0000-0002-0679-1857
Haig KeshishianMolecular, Cellular, and Developmental Biology Department, Yale University, POB 208103, New Haven, Connecticut, 06520.
Yale University · US

Funding

CELLULAR AND MOLECULAR MECHANISMS OF SYNAPTOGENESISR01NS031651 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 1993 to 2013
$4.2M
Molecular Genetic Tools for Transneuronal Transfer with TransactivationR21NS088641 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 2015 to 2016
$458k
Novel Molecular Tools for Transsynaptic Circuit AnalysisR21NS053807 · NINDS · YALE UNIVERSITY · PI KESHISHIAN, HAIG S · 2006 to 2007
$352k
NINDS NIH HHS R01 NS031651NINDS NIH HHS R21 NS053807NINDS NIH HHS R21 NS088641
6 · The paper itself

Abstract

The removal of miswired synapses is a fundamental prerequisite for normal circuit development, leading to clinical problems when aberrant. However, the underlying activity-dependent molecular mechanisms involved in synaptic pruning remain incompletely resolved. Here the dynamic properties of intracellular calcium oscillations and a role for cAMP signaling during synaptic refinement in intact Drosophila embryos were examined using optogenetic tools. We provide In vivo evidence at the single gene level that the calcium-dependent adenylyl cyclase rutabaga, the phosphodiesterase dunce, the kinase PKA, and Protein Phosphatase 1 (PP1) all operate within a functional signaling pathway to modulate Sema2a-dependent chemorepulsion. It was found that presynaptic cAMP levels were required to be dynamically maintained at an optimal level to suppress connectivity defects. It was also proposed that PP1 may serve as a molecular link between cAMP signaling and CaMKII in the pathway underlying refinement. The results introduced an in vivo model where presynaptic cAMP levels, downstream of electrical activity and calcium influx, act via PKA and PP1 to modulate the neuron's response to chemorepulsion involved in the withdrawal of off-target synaptic contacts. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 39-60, 2017.

Indexed as

3',5'-Cyclic-AMP PhosphodiesterasesAdenylyl CyclasesAnimalsCalcium SignalingCyclic AMPCyclic AMP-Dependent Protein KinasesDrosophilaDrosophila ProteinsNeuromuscular JunctionOptogeneticsProtein Phosphatase 1Signal Transduction3',5'-Cyclic-AMP PhosphodiesterasesAdenylyl CyclasesCyclic AMPCyclic AMP-Dependent Protein KinasesDrosophila ProteinsProtein Phosphatase 1activity-dependentchemorepulsioncritical periodgrowth conepruning

Identifiers

PMID27281494
PMCPMC5148738
OpenAlexW2417985985

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.