Evidence map›Paper›PMID 35465089›Full record

ArticleFrontiers in molecular neuroscience2022

Excitatory and Inhibitory Synaptic Imbalance Caused by Brain-Derived Neurotrophic Factor Deficits During Development in a Valproic Acid Mouse Model of Autism.

Chuchu Qi, Andi Chen, Honghui Mao, Erling Hu, Junye Ge, Guaiguai Ma, Keke Ren, Qian Xue, Wenting Wang, Shengxi Wu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  17. An alpha 5-GABAAutism research : official journal of the International Society for Autism Research · 2024
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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

10 authors at 3 institutions in 1 country.

Chuchu QiDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Andi ChenDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Honghui MaoDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Erling HuDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Junye GeDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Guaiguai MaDepartment of Physiology, Medical College of Yan'an University, Yan'an, China.
Keke RenDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Qian XueDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Wenting WangDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Shengxi WuDepartment of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Air Force Medical University · CNShaanxi Normal University · CNYan'an University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental factors, such as medication during pregnancy, are one of the major causes of autism spectrum disorder (ASD). Valproic acid (VPA) intake during pregnancy has been reported to dramatically elevate autism risk in offspring. Recently, researchers have proposed that VPA exposure could induce excitatory or inhibitory synaptic dysfunction. However, it remains to be determined whether and how alterations in the excitatory/inhibitory (E/I) balance contribute to VPA-induced ASD in a mouse model. In the present study, we explored changes in the E/I balance during different developmental periods in a VPA mouse model. We found that typical markers of pre- and postsynaptic excitatory and inhibitory function involved in E/I balance markedly decreased during development, reflecting difficulties in the development of synaptic plasticity in VPA-exposed mice. The expression of brain-derived neurotrophic factor (BDNF), a neurotrophin that promotes the formation and maturation of glutamatergic and GABAergic synapses during postnatal development, was severely reduced in the VPA-exposed group. Treatment with exogenous BDNF during the critical E/I imbalance period rescued synaptic functions and autism-like behaviors, such as social defects. With these results, we experimentally showed that social dysfunction in the VPA mouse model of autism might be caused by E/I imbalance stemming from BDNF deficits during the developmental stage.

Indexed as

autismBDNFE/I balanceexcitatory synapseinhibitory synapsesynaptic developmentvalproic acid

Identifiers

PMID35465089
PMCPMC9019547
OpenAlexW4226022528

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.