Evidence map›Paper›PMID 34021263›Full record

ArticleMolecular psychiatry2021

Imbalanced post- and extrasynaptic SHANK2A functions during development affect social behavior in SHANK2-mediated neuropsychiatric disorders.

Ahmed Eltokhi, Miguel A Gonzalez-Lozano, Lars-Lennart Oettl, Andrey Rozov, Claudia Pitzer, Ralph Röth, Simone Berkel, Markus Hüser, Aliona Harten, Wolfgang Kelsch and 3 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Autism patient-derived SHANK2BMolecular psychiatry · 2024
    Article
  16. Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024
    Review
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 3 countries.

Ahmed EltokhiResearch Group of the Max Planck Institute for Medical Research at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-9067-5017
Miguel A Gonzalez-Lozano *Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, Vrije University Amsterdam, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-7837-151X
Lars-Lennart Oettl *Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0003-3528-4843
Andrey Rozov *Department of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-4932-4095
Claudia PitzerInterdisciplinary Neurobiological Core (INBC), Heidelberg University, Heidelberg, Germany.
Ralph RöthDepartment of Human Molecular Genetics, Heidelberg University, Heidelberg, Germany.
Simone BerkelDepartment of Human Molecular Genetics, Heidelberg University, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5134-2217
Markus HüserResearch Group of the Max Planck Institute for Medical Research at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany.
Aliona HartenResearch Group of the Max Planck Institute for Medical Research at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany.
Wolfgang KelschCentral Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID http://orcid.org/0000-0002-3470-8125
August B SmitDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, Vrije University Amsterdam, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-2286-1587
Gudrun A RappoldDepartment of Human Molecular Genetics, Heidelberg University, Heidelberg, Germany. Gudrun.Rappold@med.uni-heidelberg.de.ORCID http://orcid.org/0000-0002-3126-1508
Rolf SprengelResearch Group of the Max Planck Institute for Medical Research at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany. Rolf.Sprengel@mpimf-heidelberg.mpg.de.ORCID http://orcid.org/0000-0003-3370-0970
Heidelberg University · DEAmsterdam Neuroscience · NLJohannes Gutenberg University Mainz · DEKazan Federal University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in SHANK genes play an undisputed role in neuropsychiatric disorders. Until now, research has focused on the postsynaptic function of SHANKs, and prominent postsynaptic alterations in glutamatergic signal transmission have been reported in Shank KO mouse models. Recent studies have also suggested a possible presynaptic function of SHANK proteins, but these remain poorly defined. In this study, we examined how SHANK2 can mediate electrophysiological, molecular, and behavioral effects by conditionally overexpressing either wild-type SHANK2A or the extrasynaptic SHANK2A(R462X) variant. SHANK2A overexpression affected pre- and postsynaptic targets and revealed a reversible, development-dependent autism spectrum disorder-like behavior. SHANK2A also mediated redistribution of Ca

Indexed as

Autism Spectrum DisorderAnimalsHippocampusMiceNerve Tissue ProteinsNeuronsReceptors, AMPASocial BehaviorNerve Tissue ProteinsReceptors, AMPAShank2 protein, mouse

Identifiers

PMID34021263
PMCPMC8760046
OpenAlexW3160147095

What OpenQuestion holds

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LicenceCC BY
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.