Evidence map›Paper›PMID 27005990›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2017

eEF2K/eEF2 Pathway Controls the Excitation/Inhibition Balance and Susceptibility to Epileptic Seizures.

Christopher Heise, Elham Taha, Luca Murru, Luisa Ponzoni, Angela Cattaneo, Fabrizia C Guarnieri, Caterina Montani, Adele Mossa, Elena Vezzoli, Giulio Ippolito and 19 more

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.2field-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

36 citing papers in PubMed, 69 citations in OpenAlex.

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  19. 4E-BP2-dependent translation in parvalbumin neurons controls epileptic seizure threshold.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Review
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

29 authors at 8 institutions in 5 countries.

Christopher HeiseCNR Neuroscience Institute, Milan, Italy.
Elham TahaSagol Department of Neurobiology, University of Haifa, Haifa, Israel.
Luca MurruCNR Neuroscience Institute, Milan, Italy.
Luisa PonzoniDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy.
Angela CattaneoIFOM-FIRC Institute of Molecular Oncology, Milan, Italy.
Fabrizia C GuarnieriDivision of Neuroscience, San Raffaele Scientific Institute and Vita-Salute University, Milan, Italy.
Caterina MontaniCNR Neuroscience Institute, Milan, Italy.
Adele MossaCNR Neuroscience Institute, Milan, Italy.
Elena VezzoliCNR Neuroscience Institute, Milan, Italy.
Giulio IppolitoCNR Neuroscience Institute, Milan, Italy.
Jonathan ZapataCNR Neuroscience Institute, Milan, Italy.
Iliana BarreraSagol Department of Neurobiology and.
Alexey G RyazanovThe Department of Pharmacology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
James CookDepartment of Chemistry and Biochemistry, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
Michael PoeDepartment of Chemistry and Biochemistry, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
Michael Rajesh StephenDepartment of Chemistry and Biochemistry, University of Wisconsin-Milwaukee, Milwaukee, WI, USA.
Maksym KopanitsaSynome, Babraham Research Campus, Cambridge CB22 3AT, UK.
Roberta BenfanteCNR Neuroscience Institute, Milan, Italy.
Francesco RusconiDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy.
Daniela BraidaDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy.
Maura FrancoliniCNR Neuroscience Institute, Milan, Italy.
Christopher G ProudUniversity of Southampton, Centre for Biological Sciences, Southampton SO17 1BJ, UK.
Flavia ValtortaDivision of Neuroscience, San Raffaele Scientific Institute and Vita-Salute University, Milan, Italy.
Maria PassafaroCNR Neuroscience Institute, Milan, Italy.
Mariaelvina SalaCNR Neuroscience Institute, Milan, Italy.
Angela BachiIFOM-FIRC Institute of Molecular Oncology, Milan, Italy.
Chiara VerpelliCNR Neuroscience Institute, Milan, Italy.
Kobi RosenblumSagol Department of Neurobiology and.
Carlo SalaCNR Neuroscience Institute, Milan, Italy, Università degli Studi di Milano, Milan, Italy.
Neuroscience Institute · ITUniversity of Milan · ITUniversity of Haifa · ILUniversity of Wisconsin–Milwaukee · USFIRC Institute of Molecular Oncology · ITVita-Salute San Raffaele University · ITSynome (United Kingdom) · GBUniversity of Adelaide · AU

Funding

Design of New Therapeutic Agents to Treat SchizophreniaR01MH096463 · NIMH · UNIVERSITY OF WISCONSIN MILWAUKEE · PI COOK, JAMES M · 2013 to 2017
$1.9M
EFFECTS OF X-RAYS ON NORMAL AND MALIGNANT CELLSR01CA004483 · NCI · WASHINGTON UNIVERSITY · PI TOLMACH, LEONARD J. · 1985 to 1988
–
Biotechnology and Biological Sciences Research Council BB/I004483/1NIMH NIH HHS R01 MH096463Wellcome TrustWellcome Trust 086688
6 · The paper itself

Abstract

Alterations in the balance of inhibitory and excitatory synaptic transmission have been implicated in the pathogenesis of neurological disorders such as epilepsy. Eukaryotic elongation factor 2 kinase (eEF2K) is a highly regulated, ubiquitous kinase involved in the control of protein translation. Here, we show that eEF2K activity negatively regulates GABAergic synaptic transmission. Indeed, loss of eEF2K increases GABAergic synaptic transmission by upregulating the presynaptic protein Synapsin 2b and α5-containing GABAA receptors and thus interferes with the excitation/inhibition balance. This cellular phenotype is accompanied by an increased resistance to epilepsy and an impairment of only a specific hippocampal-dependent fear conditioning. From a clinical perspective, our results identify eEF2K as a potential novel target for antiepileptic drugs, since pharmacological and genetic inhibition of eEF2K can revert the epileptic phenotype in a mouse model of human epilepsy.

Indexed as

AnimalsCells, CulturedCerebral CortexConditioning, PsychologicalDisease Models, AnimalElongation Factor 2 KinaseEpilepsyFeargamma-Aminobutyric AcidHippocampusMice, Inbred C57BLMice, KnockoutNeural InhibitionNeuronsRats, Sprague-DawleyReceptors, GABA-AEef2k protein, mouseEef2k protein, ratElongation Factor 2 KinaseGabra5 protein, mousegamma-Aminobutyric AcidReceptors, GABA-ASynapsinsepilepsyfear conditioningGABA receptorshippocampusinhibitory synapsestranslation elongation regulation

Identifiers

PMID27005990
PMCPMC5963824
OpenAlexW2306974599

What Socratic 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 Socratic graph.