Evidence map›Paper›PMID 27022627›Full record

ArticleeNeuro

CA3 Synaptic Silencing Attenuates Kainic Acid-Induced Seizures and Hippocampal Network Oscillations.

Lily M Y Yu, Denis Polygalov, Marie E Wintzer, Ming-Ching Chiang, Thomas J McHugh

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. International journal of molecular sciences · 2023
    Article
  6. Article
  7. Early death in a mouse model of Alzheimer's disease exacerbated by microglial loss of TAM receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Article
  10. Article
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  12. Article
  13. Review
  14. Article
  15. Review
  16. α4βδ GABANeuroscience · 2019
    Article
  17. Kainate Receptors: Role in Epilepsy.Frontiers in molecular neuroscience · 2018
    Review
  18. 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 1 institution in 1 country.

Lily M Y YuLaboratory for Circuit and Behavioral Physiology, RIKEN Brain Science Institute , Wakoshi, Saitama, Japan 351-0198.
Denis PolygalovLaboratory for Circuit and Behavioral Physiology, RIKEN Brain Science Institute , Wakoshi, Saitama, Japan 351-0198.ORCID 0000-0002-8165-5257
Marie E WintzerLaboratory for Circuit and Behavioral Physiology, RIKEN Brain Science Institute , Wakoshi, Saitama, Japan 351-0198.
Ming-Ching ChiangLaboratory for Circuit and Behavioral Physiology, RIKEN Brain Science Institute , Wakoshi, Saitama, Japan 351-0198.ORCID 0000-0002-1188-0774
Thomas J McHughLaboratory for Circuit and Behavioral Physiology, RIKEN Brain Science Institute , Wakoshi, Saitama, Japan 351-0198.
RIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a neurological disorder defined by the presence of seizure activity, manifest both behaviorally and as abnormal activity in neuronal networks. An established model to study the disorder in rodents is the systemic injection of kainic acid, an excitatory neurotoxin that at low doses quickly induces behavioral and electrophysiological seizures. Although the CA3 region of the hippocampus has been suggested to be crucial for kainic acid-induced seizure, because of its strong expression of kainate glutamate receptors and its high degree of recurrent connectivity, the precise role of excitatory transmission in CA3 in the generation of seizure and the accompanying increase in neuronal oscillations remains largely untested. Here we use transgenic mice in which CA3 pyramidal cell synaptic transmission can be inducibly silenced in the adult to demonstrate CA3 excitatory output is required for both the generation of epileptiform oscillatory activity and the progression of behavioral seizures.

Indexed as

Disease Models, AnimalAnimalsBrain WavesCA3 Region, HippocampalKainic AcidMaleMiceMice, Inbred C57BLMice, TransgenicProto-Oncogene Proteins c-fosPyramidal CellsSeizuresSynaptic TransmissionTetanus ToxinKainic AcidProto-Oncogene Proteins c-fosTetanus ToxinCA3gammahippocampuskainic acidseizuretetanus toxin

Identifiers

PMID27022627
PMCPMC4797997
OpenAlexW2269367396

What OpenQuestion holds

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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.