Evidence map›Paper›PMID 28452419›Full record

ArticleEpilepsia2017

Neurosteroid-sensitive δ-GABA

Suchitra Joshi, Karthik Rajasekaran, John Williamson, Jaideep Kapur

Open access · bronzeAbstract read
In one paragraph

Article in Epilepsia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Why ketamine.Epilepsy & behavior : E&B · 2023
    Review
  6. Virally-induced expression of GABAProgress in neurobiology · 2022
    Article
  7. Review
  8. Review
  9. Review
  10. Neurosteroids and Focal Epileptic Disorders.International journal of molecular sciences · 2020
    Review
  11. Reduced neurosteroid potentiation of GABAAnnals of clinical and translational neurology · 2020
    Article
  12. Neurosteroid regulation of GABABrain research · 2019
    Review
  13. Article
  14. Review
  15. Review
  16. 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 1 institution in 1 country.

Suchitra JoshiDepartment of Neurology, University of Virginia, Charlottesville, Virginia, U.S.A.
Karthik RajasekaranDepartment of Neurology, University of Virginia, Charlottesville, Virginia, U.S.A.
John WilliamsonDepartment of Neurology, University of Virginia, Charlottesville, Virginia, U.S.A.
Jaideep KapurDepartment of Neurology, University of Virginia, Charlottesville, Virginia, U.S.A.
University of Virginia · US

Funding

TREATMENT OF STATUS EPILEPTICUSR01NS040337 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAPUR, JAIDEEP · 2000 to 2021
$5.0M
Neurosteroid Regulation of SeizuresR01NS044370 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAPUR, JAIDEEP · 2003 to 2017
$4.1M
NINDS NIH HHS R01 NS040337NINDS NIH HHS R01 NS044370
6 · The paper itself

Abstract

objectiveWe determined the role of the neurosteroid-sensitive δ subunit-containing γ-aminobutyric acid A receptors (δ-GABARs) in epileptogenesis.

methodsStatus epilepticus (SE) was induced via lithium pilocarpine in adult rats, and seizures were assessed by continuous video-electroencephalography (EEG) monitoring. Finasteride was administered to inhibit neurosteroid synthesis. The total and surface protein expression of hippocampal δ, α4, and γ2 GABAR subunits was studied using biotinylation assays and Western blotting. Neurosteroid potentiation of the tonic currents of dentate granule cells (DGCs) was measured by whole-cell patch-clamp technique. Finally, the effects of inhibiting N-methyl-d-aspartate receptors (NMDARs) during SE on the long-term plasticity of δ-GABARs, neurosteroid-induced modulation of tonic current, and epileptogenesis were studied.

resultsThe inhibition of neurosteroid synthesis 4 days after SE triggered acute seizures and accelerated the onset of chronic recurrent spontaneous seizures (epilepsy). The down-regulation of neurosteroid-sensitive δ-GABARs occurred prior to the onset of epilepsy, whereas an increased expression of the γ2-GABAR subunits occurred after seizure onset. MK801 blockade of NMDARs during SE preserved the expression of neurosteroid-sensitive δ-GABARs. NMDAR blockade during SE also prevented the onset of spontaneous seizures. SIGNIFICANCE: Changes in neurosteroid-sensitive δ-GABAR expression correlated temporally with epileptogenesis. These findings raise the possibility that δ-GABAR plasticity may play a role in epileptogenesis.

Indexed as

AnimalsBlotting, WesternDentate GyrusDisease Models, AnimalDizocilpine MaleateDown-RegulationElectroencephalographyEpilepsy, Temporal LobeFemaleFinasterideHippocampusLithium CompoundsMaleNeuronal PlasticityNeuronsNeurotransmitter AgentsDizocilpine MaleateFinasterideLithium CompoundsNeurotransmitter AgentsPilocarpineReceptors, GABA-AReceptors, N-Methyl-D-AspartateEpileptogenesisMK‐801NeurosteroidsTonic currentδ Subunit–containing GABARs

Identifiers

PMID28452419
PMCPMC5412084
OpenAlexW2573034930

What OpenQuestion holds

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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.