Evidence map›Paper›PMID 24760837›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Role of GluK1 kainate receptors in seizures, epileptic discharges, and epileptogenesis.

Brita Fritsch, Janine Reis, Maciej Gasior, Rafal M Kaminski, Michael A Rogawski

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 21% 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, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. International journal of molecular sciences · 2023
    Article
  8. Kainate Receptor Antagonists: Recent Advances and Therapeutic Perspective.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Kainate Receptors: Role in Epilepsy.Frontiers in molecular neuroscience · 2018
    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

5 authors at 2 institutions in 2 countries.

Brita FritschEpilepsy Research Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, Department of Neurology, University Hospital, 79106 Freiburg, Germany, and Department of Neurology, School of Medicine and Center for Neuroscience, University of California, Davis, Sacramento, California 95817.
Janine Reis
Maciej Gasior
Rafal M Kaminski
Michael A Rogawski
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Identification of novel therapeutic approaches for TETS and OP intoxicationR21NS072094 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEIN, PAMELA J, ROGAWSKI, MICHAEL A. · 2010 to 2011
$767k
Intramural NIH HHSNINDS NIH HHS NS072094NINDS NIH HHS NS079292NINDS NIH HHS R21 NS072094
6 · The paper itself

Abstract

Kainate receptors containing the GluK1 subunit have an impact on excitatory and inhibitory neurotransmission in brain regions, such as the amygdala and hippocampus, which are relevant to seizures and epilepsy. Here we used 2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid (ATPA), a potent and selective agonist of kainate receptors that include the GluK1 subunit, in conjunction with mice deficient in GluK1 and GluK2 kainate receptor subunits to assess the role of GluK1 kainate receptors in provoking seizures and in kindling epileptogenesis. We found that systemic ATPA, acting specifically via GluK1 kainate receptors, causes locomotor arrest and forelimb extension (a unique behavioral characteristic of GluK1 activation) and induces myoclonic behavioral seizures and electrographic seizure discharges in the BLA and hippocampus. In contrast, the proconvulsant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1 kainate receptors, and deletion of these receptors does not elevate the threshold for seizures in the 6 Hz model. ATPA also specifically activates epileptiform discharges in BLA slices in vitro via GluK1 kainate receptors. Olfactory bulb kindling developed similarly in wild-type, GluK1, and GluK2 knock-out mice, demonstrating that GluK1 kainate receptors are not required for epileptogenesis or seizure expression in this model. We conclude that selective activation of kainate receptors containing the GluK1 subunit can trigger seizures, but these receptors are not necessary for seizure generation in models commonly used to identify therapeutic agents for the treatment of epilepsy.

Indexed as

AmygdalaAnimalsEpilepsyExcitatory Amino Acid AgonistsGluK2 Kainate ReceptorHippocampusIsoxazolesKainic Acid ReceptorsMiceMice, KnockoutPropionatesRatsRats, Sprague-DawleySeizuresalpha-amino-3-hydroxy-5-tert-butyl-4-isoxazolepropionateExcitatory Amino Acid AgonistsGluK2 Kainate ReceptorIsoxazolesKainic Acid ReceptorsPropionatesATPABLAepilepsykainate receptorkindlingseizure

Identifiers

PMID24760837
PMCPMC3996208
OpenAlexW1977504030

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.