Evidence map›Paper›PMID 19295155›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Cellular plasticity for group I mGluR-mediated epileptogenesis.

Riccardo Bianchi, Shih-Chieh Chuang, Wangfa Zhao, Steven R Young, Robert K S Wong

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. CRISPR-mediated activation of autism geneMolecular therapy. Nucleic acids · 2022
    Article
  3. Article
  4. Article
  5. Hyperexcitability and Homeostasis in Fragile X Syndrome.Frontiers in molecular neuroscience · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. 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 1 country.

Riccardo BianchiThe Robert F. Furchgott Center for Neural and Behavioral Science and Department of Physiology and Pharmacology, State University of New York Downstate Medical Center, Brooklyn, New York 11203, USA. rbianchi@downstate.edu
Shih-Chieh Chuang
Wangfa Zhao
Steven R Young
Robert K S Wong
SUNY Downstate Health Sciences University · USState University of New York · US

Funding

GLUTAMATE RECEPTORS IN EPILEPSYR01NS035481 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI WONG, ROBERT K · 1998 to 2011
$3.0M
Glutamate Receptors in EpilepsyR56NS035481 · NINDS · SUNY DOWNSTATE MEDICAL CENTER · PI WONG, ROBERT K · 2008 to 2008
$390k
NINDS NIH HHS NS35481NINDS NIH HHS R01 NS035481NINDS NIH HHS R56 NS035481
6 · The paper itself

Abstract

Stimulation of group I metabotropic glutamate receptors (mGluRs) by the agonist (S)-dihydroxyphenylglycine in the hippocampus transforms normal neuronal activity into prolonged epileptiform discharges. The conversion is long lasting in that epileptiform discharges persist after washout of the inducing agonist and serves as a model of epileptogenesis. The group I mGluR model of epileptogenesis took on special significance because epilepsy associated with fragile X syndrome (FXS) may be caused by excessive group I mGluR signaling. At present, the plasticity mechanism underlying the group I mGluR-mediated epileptogenesis is unknown. I(mGluR(V)), a voltage-gated cationic current activated by group I mGluR agonists in CA3 pyramidal cells in the hippocampus, is a possible candidate. I(mGluR(V)) activation is associated with group I mGluR agonist-elicited epileptiform discharges. For I(mGluR(V)) to play a role in epileptogenesis, long-term activation of the current must occur after group I mGluR agonist exposure or synaptic stimulation. We observed that I(mGluR(V)), once induced by group I mGluR agonist stimulation in CA3 pyramidal cells, remained undiminished for hours after agonist washout. In slices prepared from FXS model mice, repeated stimulation of recurrent CA3 pyramidal cell synapses, effective in eliciting mGluR-mediated epileptiform discharges, also induced long-lasting I(mGluR(V)) in CA3 pyramidal cells. Similar to group I mGluR-mediated prolonged epileptiform discharges, persistent I(mGluR(V)) was no longer observed in preparations pretreated with inhibitors of tyrosine kinase, of extracellular signal-regulated kinase 1/2, or of mRNA protein synthesis. The results indicate that I(mGluR(V)) is an intrinsic plasticity mechanism associated with group I mGluR-mediated epileptogenesis.

Indexed as

AnimalsEpilepsyExcitatory Amino Acid AgonistsGuinea PigsMiceMice, TransgenicNeuronal PlasticityPyramidal CellsReceptors, Metabotropic GlutamateSignal TransductionExcitatory Amino Acid Agonistsmetabotropic glutamate receptor type 1Receptors, Metabotropic Glutamate

Identifiers

PMID19295155
PMCPMC2692254
OpenAlexW1990784803

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.