Evidence map›Paper›PMID 30635860›Full record

ArticleMolecular neurobiology2019

Deletion of Semaphorin 3F in Interneurons Is Associated with Decreased GABAergic Neurons, Autism-like Behavior, and Increased Oxidative Stress Cascades.

Zhu Li, Rekha Jagadapillai, Evelyne Gozal, Gregory Barnes

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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  14. Review
  15. Review
  16. Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021
    Review
  17. Novel Truncating and Missense Variants inFrontiers in cell and developmental biology · 2021
    Article
  18. Article
  19. Expression of Genes Involved in Axon Guidance: How Much Have We Learned?International journal of molecular sciences · 2020
    Review
  20. Article
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

4 authors at 2 institutions in 1 country.

Zhu LiDepartment of Neurology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Rekha JagadapillaiDepartment of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Evelyne GozalDepartment of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA.
Gregory BarnesDepartment of Pediatrics, University of Louisville School of Medicine, Louisville, KY, USA. Gregory.barnes@louisville.edu.ORCID http://orcid.org/0000-0002-7711-5506
University of Louisville · USVanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism and epilepsy are diseases which have complex genetic inheritance. Genome-wide association and other genetic studies have implicated at least 500+ genes associated with the occurrence of autism spectrum disorders (ASD) including the human semaphorin 3F (Sema 3F) and neuropilin 2 (NRP2) genes. However, the genetic basis of the comorbid occurrence of autism and epilepsy is unknown. The aberrant development of GABAergic circuitry is a possible risk factor in autism and epilepsy. Molecular biological approaches were used to test the hypothesis that cell-specific genetic variation in mouse homologs affects the formation and function of GABAergic circuitry. The empirical analysis with mice homozygous null for one of these genes, Sema 3F, in GABAergic neurons substantiated these predictions. Notably, deletion of Sema 3F in interneurons but not excitatory neurons during early development decreased the number of interneurons/neurites and mRNAs for cell-specific GABAergic markers and increased epileptogenesis and autistic behaviors. Studies of interneuron cell-specific knockout of Sema 3F signaling suggest that deficient Sema 3F signaling may lead to neuroinflammation and oxidative stress. Further studies of mouse KO models of ASD genes such as Sema 3F or NRP2 may be informative to clinical phenotypes contributing to the pathogenesis in autism and epilepsy patients.

Indexed as

Behavior, AnimalOxidative StressAnimalsAutistic DisorderBiomarkersCell CountEpilepsyGABAergic NeuronsGene DeletionInflammationInterneuronsMembrane ProteinsMice, Inbred C57BLMice, KnockoutMutationNerve Tissue ProteinsBiomarkersMembrane ProteinsNerve Tissue ProteinsReactive Oxygen SpeciesSema3f protein, mouseAutismDevelopmentEpilepsyHippocampusInterneuronSemaphorin

Identifiers

PMID30635860
PMCPMC6614133
OpenAlexW2909864820

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.