Evidence map›Paper›PMID 28609458›Full record

ArticlePloS one2017

Dendritic overgrowth and elevated ERK signaling during neonatal development in a mouse model of autism.

Ning Cheng, Fawaz Alshammari, Elizabeth Hughes, Maryam Khanbabaei, Jong M Rho

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  14. Mass Generation, Neuron Labeling, and 3D Imaging of Minibrains.Frontiers in bioengineering and biotechnology · 2020
    Article
  15. Hippocampal deficits in neurodevelopmental disorders.Neurobiology of learning and memory · 2019
    Review
  16. Article
  17. Review
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  19. International journal of molecular sciences · 2019
    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

5 authors at 1 institution in 1 country.

Ning ChengDevelopmental Neurosciences Research Program, Alberta Children's Hospital Research Institute (ACHRI), Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID http://orcid.org/0000-0003-0300-9791
Fawaz AlshammariO'Brien Centre for the Bachelor of Health Sciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Elizabeth HughesDevelopmental Neurosciences Research Program, Alberta Children's Hospital Research Institute (ACHRI), Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Maryam KhanbabaeiDevelopmental Neurosciences Research Program, Alberta Children's Hospital Research Institute (ACHRI), Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Jong M RhoDepartments of Pediatrics, Clinical Neurosciences, Physiology & Pharmacology, Alberta Children's Hospital Research Institute (ACHRI), Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (hereafter referred to as "ASD") is a heterogeneous neurodevelopmental condition characterized by impaired social communication and interactions, and restricted, repetitive activities or interests. Alterations in network connectivity and memory function are frequently observed in autism patients, often involving the hippocampus. However, specific changes during early brain development leading to disrupted functioning remain largely unclear. Here, we investigated the development of dendritic arbor of hippocampal CA1 pyramidal neurons in the BTBR T+tf/J (BTBR) mouse model of autism. BTBR mice display the defining behavioural features of autism, and also exhibit impaired learning and memory. We found that compared to control C57BL/6J (B6) animals, the lengths of both apical and basal dendrites were significantly greater in neonatal BTBR animals. Further, basal dendrites in the BTBR mice had higher branching complexity. In contrast, cross-sectional area of the soma was unchanged. In addition, we observed a similar density of CA1 pyramidal neurons and thickness of the neuronal layer between the two strains. Thus, there was a specific, compartmentalized overgrowth of dendrites during early development in the BTBR animals. Biochemical analysis further showed that the extracellular signal-regulated kinases (ERK) pathway was up-regulated in the hippocampus of neonatal BTBR animals. Since dendritic structure is critical for information integration and relay, our data suggest that altered development of dendrites could potentially contribute to impaired hippocampal function and behavior observed in the BTBR model, and that this might be related to increased activation of the ERK pathway.

Indexed as

Disease Models, AnimalAnimalsAnimals, NewbornAutism Spectrum DisorderBlotting, WesternCA1 Region, HippocampalDendritesExtracellular Signal-Regulated MAP KinasesImmunohistochemistryLearning DisabilitiesMAP Kinase Signaling SystemMemory DisordersMice, Inbred C57BLMicroscopy, ConfocalPyramidal CellsExtracellular Signal-Regulated MAP Kinases

Identifiers

PMID28609458
PMCPMC5469475
OpenAlexW2625729136

What OpenQuestion 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 OpenQuestion graph.