Evidence map›Paper›PMID 31645553›Full record

ArticleNature communications2019

Cellular and synaptic phenotypes lead to disrupted information processing in Fmr1-KO mouse layer 4 barrel cortex.

Aleksander P F Domanski, Sam A Booker, David J A Wyllie, John T R Isaac, Peter C Kind

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

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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

5 authors.

Aleksander P F DomanskiSchool of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, UK. aleks.domanski@bristol.ac.uk.ORCID http://orcid.org/0000-0001-9582-5192
Sam A BookerCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.
David J A WyllieCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK.ORCID http://orcid.org/0000-0002-4957-6049
John T R IsaacDevelopmental Synaptic Plasticity Section, NINDS, NIH, Bethesda, MD, 20892, USA. jisaac5@ITS.JNJ.com.
Peter C KindCentre for Discovery Brain Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, EH8 9XD, UK. pkind@ed.ac.uk.

Funding

Medical Research Council G0300466Medical Research Council G0601584Medical Research Council G0700967Medical Research Council MR/K014137/1Medical Research Council MR/P006213/1Wellcome Trust
6 · The paper itself

Abstract

Sensory hypersensitivity is a common and debilitating feature of neurodevelopmental disorders such as Fragile X Syndrome (FXS). How developmental changes in neuronal function culminate in network dysfunction that underlies sensory hypersensitivities is unknown. By systematically studying cellular and synaptic properties of layer 4 neurons combined with cellular and network simulations, we explored how the array of phenotypes in Fmr1-knockout (KO) mice produce circuit pathology during development. We show that many of the cellular and synaptic pathologies in Fmr1-KO mice are antagonistic, mitigating circuit dysfunction, and hence may be compensatory to the primary pathology. Overall, the layer 4 network in the Fmr1-KO exhibits significant alterations in spike output in response to thalamocortical input and distorted sensory encoding. This developmental loss of layer 4 sensory encoding precision would contribute to subsequent developmental alterations in layer 4-to-layer 2/3 connectivity and plasticity observed in Fmr1-KO mice, and circuit dysfunction underlying sensory hypersensitivity.

Indexed as

Action PotentialsAnimalsComputer SimulationDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGlutamic AcidMaleMiceMice, KnockoutNeuronsPatch-Clamp TechniquesPhenotypeSomatosensory CortexSynapsesFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Glutamic Acid

Identifiers

PMID31645553
PMCPMC6811545

What OpenQuestion holds

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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.