Evidence map›Paper›PMID 30605686›Full record

ArticleCell reports2019

Augmented Reticular Thalamic Bursting and Seizures in Scn1a-Dravet Syndrome.

Stefanie Ritter-Makinson, Alexandra Clemente-Perez, Bryan Higashikubo, Frances S Cho, Stephanie S Holden, Eric Bennett, Ana Chkhaidze, Oscar H J Eelkman Rooda, Marie-Coralie Cornet, Freek E Hoebeek and 4 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.8field-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

40 citing papers in PubMed, 65 citations in OpenAlex.

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  12. Modified human mesenchymal stromal/stem cells restore cortical excitability after focal ischemic stroke in rats.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 5 countries.

Stefanie Ritter-MakinsonGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Alexandra Clemente-PerezGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Neurosciences Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA.
Bryan HigashikuboGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Frances S ChoGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Neurosciences Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA.
Stephanie S HoldenGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Physiology, University of California, San Francisco, San Francisco, CA 94158, USA; Neurosciences Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA.
Eric BennettGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Ana ChkhaidzeGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Oscar H J Eelkman RoodaDepartment of Neuroscience, Erasmus MC, Rotterdam, the Netherlands; Department of Neurosurgery, Erasmus MC, Rotterdam, the Netherlands.
Marie-Coralie CornetDepartment of Pediatrics, University of California, San Francisco, San Francisco, CA 94158, USA; Department of Pediatrics, Catholic University of Louvain, Louvain, Belgium.
Freek E HoebeekDepartment of Neuroscience, Erasmus MC, Rotterdam, the Netherlands; Department of Neurosurgery, Erasmus MC, Rotterdam, the Netherlands; NIDOD Institute, Wilhelmina Children's Hospital, University Medical Center Utrecht and Brain Center Rudolf Magnus, Utrecht, the Netherlands.
Kazuhiro YamakawaLaboratory for Neurogenetics, RIKEN Brain Science Institute, Wako, Japan.
Maria Roberta CilioDepartment of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA.
Bruno DelordInstitut des Systèmes Intelligents et de Robotique (ISIR), Sorbonne University, 4 Place Jussieu, 75005 Paris, France.
Jeanne T PazGladstone Institute of Neurological Disease, San Francisco, San Francisco, CA 94158, USA; Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA; Neurosciences Graduate Program, University of California, San Francisco, San Francisco, CA 94158, USA; Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: jeanne.paz@gladstone.ucsf.edu.
Gladstone Institutes · USUniversity of California, San Francisco · USErasmus University Rotterdam · NLRIKEN Center for Brain Science · JPSorbonne Université · FRUCLouvain · BE

Funding

The Role of Inflammation in Post-stroke EpileptogenesisR01NS096369 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI PAZ, JEANNE T · 2016 to 2021
$2.3M
Role of Thalamus in Post-stroke epileptogenesisR00NS078118 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI PAZ, JEANNE T · 2014 to 2016
$747k
NINDS NIH HHS R00 NS078118NINDS NIH HHS R01 NS096369
6 · The paper itself

Abstract

Loss of function in the Scn1a gene leads to a severe epileptic encephalopathy called Dravet syndrome (DS). Reduced excitability in cortical inhibitory neurons is thought to be the major cause of DS seizures. Here, in contrast, we show enhanced excitability in thalamic inhibitory neurons that promotes the non-convulsive seizures that are a prominent yet poorly understood feature of DS. In a mouse model of DS with a loss of function in Scn1a, reticular thalamic cells exhibited abnormally long bursts of firing caused by the downregulation of calcium-activated potassium SK channels. Our study supports a mechanism in which loss of SK activity causes the reticular thalamic neurons to become hyperexcitable and promote non-convulsive seizures in DS. We propose that reduced excitability of inhibitory neurons is not global in DS and that non-GABAergic mechanisms such as SK channels may be important targets for treatment.

Indexed as

AnimalsDisease Models, AnimalEpilepsies, MyoclonicHumansMiceSeizuresThalamusDravet syndromeepilepsyNav1.1optogeneticsreticular thalamic nucleusScn1aseizuresSK currentthalamocortical circuitsthalamocortical oscillations

Identifiers

PMID30605686
PMCPMC6555418
OpenAlexW2907719702

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.