Evidence map›Paper›PMID 23277570›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Neuronal Nogo-A negatively regulates dendritic morphology and synaptic transmission in the cerebellum.

Marija M Petrinovic, Raphael Hourez, Elisabeth M Aloy, Gregoire Dewarrat, David Gall, Oliver Weinmann, Julien Gaudias, Lukas C Bachmann, Serge N Schiffmann, Kaspar E Vogt and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Nogo-A is secreted in extracellular vesicles, occurs in blood and can influence vascular permeability.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  3. Article
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  5. Circuit formation in the adult brain.The European journal of neuroscience · 2022
    Review
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  7. Review
  8. Article
  9. Effects of Nogo-A and its receptor on the repair of sciatic nerve injury in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
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  11. Review
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  14. Improved functional outcome after chronic stroke with delayed anti-Nogo-A therapy: A clinically relevant intention-to-treat analysis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
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  17. Review
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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

11 authors at 4 institutions in 2 countries.

Marija M PetrinovicBrain Research Institute, University of Zürich, 8057 Zürich, Switzerland. marija-magdalena.petrinovic@roche.com
Raphael Hourez
Elisabeth M Aloy
Gregoire Dewarrat
David Gall
Oliver Weinmann
Julien Gaudias
Lukas C Bachmann
Serge N Schiffmann
Kaspar E Vogt
Martin E Schwab
ETH Zurich · CHUniversité Libre de Bruxelles · BEUniversity of Zurich · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal signal integration as well as synaptic transmission and plasticity highly depend on the morphology of dendrites and their spines. Nogo-A is a membrane protein enriched in the adult central nervous system (CNS) myelin, where it restricts the capacity of axons to grow and regenerate after injury. Nogo-A is also expressed by certain neurons, in particular during development, but its physiological function in this cell type is less well understood. We addressed this question in the cerebellum, where Nogo-A is transitorily highly expressed in the Purkinje cells (PCs) during early postnatal development. We used general genetic ablation (KO) as well as selective overexpression of Nogo-A in PCs to analyze its effect on dendritogenesis and on the formation of their main input synapses from parallel (PFs) and climbing fibers (CFs). PC dendritic trees were larger and more complex in Nogo-A KO mice and smaller than in wild-type in Nogo-A overexpressing PCs. Nogo-A KO resulted in premature soma-to-dendrite translocation of CFs and an enlargement of the CF territory in the molecular layer during development. Although spine density was not influenced by Nogo-A, the size of postsynaptic densities of PF-PC synapses was negatively correlated with the Nogo-A expression level. Electrophysiological studies revealed that Nogo-A negatively regulates the strength of synaptic transmission at the PF-PC synapse. Thus, Nogo-A appears as a negative regulator of PC input synapses, which orchestrates cerebellar connectivity through regulation of synapse morphology and the size of the PC dendritic tree.

Indexed as

AnimalsCerebellumDendritesElectrophysiological PhenomenaGene Expression Regulation, DevelopmentalGPI-Linked ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMyelin ProteinsNeuronsNogo ProteinsNogo Receptor 1Purkinje CellsReceptors, Cell SurfaceGPI-Linked ProteinsMyelin ProteinsNogo ProteinsNogo Receptor 1Receptors, Cell SurfaceRtn4 protein, mouseRtn4r protein, mouse

Identifiers

PMID23277570
PMCPMC3549069
OpenAlexW2151573576

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.