Evidence map›Paper›PMID 32909150›Full record

ArticleMolecular neurobiology2021

GABAergic Interneuron and Neurotransmission Are mTOR-Dependently Disturbed in Experimental Focal Cortical Dysplasia.

Shaoping Zhong, Zhihao Zhao, Wanjing Xie, Yiying Cai, Yiying Zhang, Jing Ding, Xin Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 20% 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, 34 citations in OpenAlex.

  1. Review
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  6. Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025
    Article
  7. Review
  8. Spatial transcriptomics in focal cortical dysplasia type IIb.Acta neuropathologica communications · 2024
    Article
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  10. Review
  11. 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

7 authors at 2 institutions in 2 countries.

Shaoping ZhongDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Zhihao ZhaoDepartment of The State Key Laboratory of Medical Neurobiology, The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
Wanjing XieDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Yiying CaiDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Yiying ZhangDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Jing DingDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China. ding.jing@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0001-5135-4210
Xin WangDepartment of Neurology, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, China. wang.xin@zs-hospital.sh.cn.
Fudan University · CNAllen Institute for Brain Science · US

Funding

National Natural Science Foundation of China 3177118National Natural Science Foundation of China 81771308
6 · The paper itself

Abstract

Focal cortical dysplasia (FCD) is a major cause for drug-resistant epilepsies. The molecular and cellular mechanisms of epileptogenesis in FCD are still poorly understood. Some studies have suggested that deficiencies of γ-aminobutyric acid (GABA) system may play an important role in type II FCD, but it remains controversial. In order to examine whether and how GABAergic interneurons and synaptic function are affected, we generated a somatic mTOR hyperactivation-based mouse model of type II FCD by in utero electroporation, quantified densities of interneurons in the malformed cortices, and recorded miniature inhibitory postsynaptic currents in dysmorphic neurons. We detected 20-25% reduction of GABAergic interneurons within malformed cortices, independent of cortical regions and cell subtypes but proportionate to the decrease of global neuron counts. GABAergic synaptic transmission from interneurons to mTOR hyperactivated dysmorphic neurons was dramatically disrupted, outweighing the decrease of interneuron counts. Postnatal mTOR inhibition partially rescued these alterations of GABAergic system. We also quantified the expression of GABA

Indexed as

Synaptic TransmissionAnimalsAnimals, NewbornDisease Models, AnimalGABAergic NeuronsGene Expression ProfilingGene Expression RegulationInhibitory Postsynaptic PotentialsInterneuronsMalformations of Cortical DevelopmentMice, TransgenicNeocortexSirolimusTOR Serine-Threonine KinasesSirolimusTOR Serine-Threonine KinasesEpilepsyFocal cortical dysplasiaGABAInterneuronmTOR pathway

Identifiers

PMID32909150
OpenAlexW3086930903

What OpenQuestion holds

Textmetadata
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.