Evidence map›Paper›PMID 38015349›Full record

ArticleNeuroscience bulletin2024

Developmental Impairments of Synaptic Refinement in the Thalamus of a Mouse Model of Fragile X Syndrome.

Xiaotong Wu, Yali Liu, Xiaomeng Wang, Lu Zheng, Libiao Pan, Hao Wang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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 1 institution in 2 countries.

Xiaotong Wu *Department of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China.ORCID https://orcid.org/0000-0001-8979-4780
Yali Liu *Department of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Xiaomeng WangDepartment of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China.ORCID https://orcid.org/0009-0004-9814-6581
Lu ZhengDepartment of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Libiao PanDepartment of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Hao WangDepartment of Neurosurgery of Second Affiliated Hospital and School of Brain Science and Brain Medicine, Key Laboratory for Biomedical Engineering of Education Ministry, Zhejiang University School of Medicine, Hangzhou, 310058, China. haowang@zju.edu.cn.ORCID https://orcid.org/0000-0003-1862-8229
Allen Institute for Brain Science · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While somatosensory over-reactivity is a common feature of autism spectrum disorders such as fragile X syndrome (FXS), the thalamic mechanisms underlying this remain unclear. Here, we found that the developmental elimination of synapses formed between the principal nucleus of V (PrV) and the ventral posterior medial nucleus (VPm) of the somatosensory system was delayed in fragile X mental retardation 1 gene knockout (Fmr1 KO) mice, while the developmental strengthening of these synapses was disrupted. Immunohistochemistry showed excessive VGluT2 puncta in mutants at P12-13, but not at P7-8 or P15-16, confirming a delay in somatic pruning of PrV-VPm synapses. Impaired synaptic function was associated with a reduction in the frequency of quantal AMPA events, as well as developmental deficits in presynaptic vesicle size and density. Our results uncovered the developmental impairment of thalamic relay synapses in Fmr1 KO mice and suggest that a thalamic contribution to the somatosensory over-reactivity in FXS should be considered.

Indexed as

Autism Spectrum DisorderFragile X SyndromeAnimalsDisease Models, AnimalFragile X Messenger Ribonucleoprotein 1MiceMice, KnockoutSynapsesThalamusFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Fragile X syndromeSensory over-reactivitySynaptic refinementVPm

Identifiers

PMID38015349
PMCPMC11004103
OpenAlexW4389084823

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.