Evidence map›Paper›PMID 23683707›Full record

ReviewSeizure2013

Molecular mechanisms of antiseizure drug activity at GABAA receptors.

L John Greenfield

Open access · hybridAbstract readReview
In one paragraph

Review in Seizure, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 2 pooled it
3.7field-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

97 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Enhancing KCC2 function reduces interictal activity and prevents seizures in temporal lobe epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Review
  14. Identification and quantification of GABAIBRO neuroscience reports · 2025
    Article
  15. Review
  16. Carvone derived cannabidiol enantiomers as novel anticonvulsants.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. Review

37 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

L John GreenfieldDept. of Neurology, University of Arkansas for Medical Sciences, 4301W. Markham St., Slot 500, Little Rock, AR 72205, United States. ljgreenfield@uams.edu.
University of Arkansas for Medical Sciences · US

Funding

Post-Hypoxic Regulation of GABA-A Receptor FunctionR01NS049389 · NINDS · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI HOWARD, MARTHE J · 2006 to 2010
$1.3M
NINDS NIH HHS R01 NS049389
6 · The paper itself

Abstract

The GABAA receptor (GABAAR) is a major target of antiseizure drugs (ASDs). A variety of agents that act at GABAARs s are used to terminate or prevent seizures. Many act at distinct receptor sites determined by the subunit composition of the holoreceptor. For the benzodiazepines, barbiturates, and loreclezole, actions at the GABAAR are the primary or only known mechanism of antiseizure action. For topiramate, felbamate, retigabine, losigamone and stiripentol, GABAAR modulation is one of several possible antiseizure mechanisms. Allopregnanolone, a progesterone metabolite that enhances GABAAR function, led to the development of ganaxolone. Other agents modulate GABAergic "tone" by regulating the synthesis, transport or breakdown of GABA. GABAAR efficacy is also affected by the transmembrane chloride gradient, which changes during development and in chronic epilepsy. This may provide an additional target for "GABAergic" ASDs. GABAAR subunit changes occur both acutely during status epilepticus and in chronic epilepsy, which alter both intrinsic GABAAR function and the response to GABAAR-acting ASDs. Manipulation of subunit expression patterns or novel ASDs targeting the altered receptors may provide a novel approach for seizure prevention.

Indexed as

AnimalsAnticonvulsantsBarbituratesBenzodiazepinesHumansReceptors, GABA-ASeizuresAnticonvulsantsBarbituratesBenzodiazepinesReceptors, GABA-AAntiepileptic drugsChloride channelEpilepsyGABA receptorInhibitionSeizures

Identifiers

PMID23683707
PMCPMC3766376
OpenAlexW2162230460

What OpenQuestion holds

Textmetadata
LicenceTDM
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.