Evidence map›Paper›PMID 25225107›Full record

ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2014

Modulation of network activity and induction of homeostatic synaptic plasticity by enzymatic removal of heparan sulfates.

Svetlana Korotchenko, Lorenzo A Cingolani, Tatiana Kuznetsova, Luca Leonardo Bologna, Michela Chiappalone, Alexander Dityatev

Open access · bronzeAbstract read
In one paragraph

Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014. 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
1.4field-weighted citation impact, top 22% 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, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. CRISPR-mediated activation of autism geneMolecular therapy. Nucleic acids · 2022
    Article
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  8. Review
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  12. Article
  13. Brain circuitry outside the synaptic cleft.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    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

6 authors at 3 institutions in 3 countries.

Svetlana KorotchenkoDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy Laboratory for Brain ECM Research, State University of Nizhny Novgorod, 603950 Nizhny Novgorod, Russia.
Lorenzo A CingolaniDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy.
Tatiana KuznetsovaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy.
Luca Leonardo BolognaINSERM, U968, Paris 75012, France Sorbonne Universités, UPMC Univ Paris 06, UMR_S 968, Institut de la Vision, Paris 75012, France CNRS, UMR_7210, Paris 75012, France.
Michela ChiappaloneDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy.
Alexander DityatevDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genoa, Italy Laboratory for Brain ECM Research, State University of Nizhny Novgorod, 603950 Nizhny Novgorod, Russia Molecular Neuroplasticity Group, German Center for Neurodegenerative Diseases (DZNE), 39120 Magdeburg, Germany alexander.dityatev@dzne.de.
Italian Institute of Technology · ITGerman Center for Neurodegenerative Diseases · DESorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heparan sulfates (HSs) are complex and highly active molecules that are required for synaptogenesis and long-term potentiation. A deficit in HSs leads to autistic phenotype in mice. Here, we investigated the long-term effect of heparinase I, which digests highly sulfated HSs, on the spontaneous bioelectrical activity of neuronal networks in developing primary hippocampal cultures. We found that chronic heparinase treatment led to a significant reduction of the mean firing rate of neurons, particularly during the period of maximal neuronal activity. Furthermore, firing pattern in heparinase-treated cultures often appeared as epileptiform bursts, with long periods of inactivity between them. These changes in network activity were accompanied by an increase in the frequency and amplitude of miniature postsynaptic excitatory currents, which could be described by a linear up-scaling of current amplitudes. Biochemically, we observed an upregulation in the expression of the glutamate receptor subunit GluA1, but not GluA2, and a strong increase in autophosphorylation of α and β Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), without changes in the levels of kinase expression. These data suggest that a deficit in HSs triggers homeostatic synaptic plasticity and drastically affects functional maturation of neural network.

Indexed as

AnimalsBlotting, WesternGene Expression RegulationHeparan SulfateHeparin LyaseHippocampusHomeostasisMiceMicroelectrodesNeuronal PlasticityNeuronsPatch-Clamp TechniquesPhosphorylationReceptors, AMPAHeparan SulfateHeparin LyaseReceptors, AMPAAMPA receptorburstheparan sulfate proteoglycansneural networkseizuresynaptic upscaling

Identifiers

PMID25225107
PMCPMC4173299
OpenAlexW2164340052

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.