Evidence map›Paper›PMID 33347690›Full record

ArticleGenes, brain, and behavior2021

Learning and reaction times in mouse touchscreen tests are differentially impacted by mutations in genes encoding postsynaptic interacting proteins SYNGAP1, NLGN3, DLGAP1, DLGAP2 and SHANK2.

Alexa E Horner, Rebecca H Norris, Robbie McLaren-Jones, Liam Alexander, Noboru H Komiyama, Seth G N Grant, Jess Nithianantharajah, Maksym V Kopanitsa

Open access · hybridAbstract read
In one paragraph

Article in Genes, brain, and behavior, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Alexa E HornerSynome Ltd, Babraham Research Campus, Cambridge, UK.
Rebecca H NorrisFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia.
Robbie McLaren-JonesSynome Ltd, Babraham Research Campus, Cambridge, UK.
Liam AlexanderSynome Ltd, Babraham Research Campus, Cambridge, UK.
Noboru H KomiyamaGenes to Cognition Programme, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Seth G N GrantGenes to Cognition Programme, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Jess NithianantharajahFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia.
Maksym V KopanitsaSynome Ltd, Babraham Research Campus, Cambridge, UK.ORCID 0000-0001-8694-9644
Babraham Institute · GBThe University of Melbourne · AUUniversity of Edinburgh · GB

Funding

European Research Council 695568Medical Research CouncilWellcome Trust 202932
6 · The paper itself

Abstract

The postsynaptic terminal of vertebrate excitatory synapses contains a highly conserved multiprotein complex that comprises neurotransmitter receptors, cell-adhesion molecules, scaffold proteins and enzymes, which are essential for brain signalling and plasticity underlying behaviour. Increasingly, mutations in genes that encode postsynaptic proteins belonging to the PSD-95 protein complex, continue to be identified in neurodevelopmental disorders (NDDs) such as autism spectrum disorder, intellectual disability and epilepsy. These disorders are highly heterogeneous, sharing genetic aetiology and comorbid cognitive and behavioural symptoms. Here, by using genetically engineered mice and innovative touchscreen-based cognitive testing, we sought to investigate whether loss-of-function mutations in genes encoding key interactors of the PSD-95 protein complex display shared phenotypes in associative learning, updating of learned associations and reaction times. Our genetic dissection of mice with loss-of-function mutations in Syngap1, Nlgn3, Dlgap1, Dlgap2 and Shank2 showed that distinct components of the PSD-95 protein complex differentially regulate learning, cognitive flexibility and reaction times in cognitive processing. These data provide insights for understanding how human mutations in these genes lead to the manifestation of diverse and complex phenotypes in NDDs.

Indexed as

LearningLoss of Function MutationAnimalsCell Adhesion Molecules, NeuronalFemaleMaleMembrane ProteinsMiceMice, Inbred C57BLNerve Tissue Proteinsras GTPase-Activating ProteinsReaction TimeSAP90-PSD95 Associated ProteinsCell Adhesion Molecules, NeuronalDlgap1 protein, mouseDlgap2 protein, mouseMembrane ProteinsNerve Tissue Proteinsneuroligin 3ras GTPase-Activating ProteinsSAP90-PSD95 Associated ProteinsShank2 protein, mouseSyngap1 protein, mouseautismDlgap1Dlgap2intellectual disabilityNlgn3postsynaptic densityreversal learningShank2Syngap1visual discrimination

Identifiers

PMID33347690
PMCPMC7615670
OpenAlexW3117999865

What Socratic holds

Textmetadata
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 Socratic graph.