Evidence map›Paper›PMID 30169757›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2018

Ca2+ Signals in Astrocytes Facilitate Spread of Epileptiform Activity.

Kjell Heuser, Cecilie G Nome, Klas H Pettersen, Knut S Åbjørsbråten, Vidar Jensen, Wannan Tang, Rolf Sprengel, Erik Taubøll, Erlend A Nagelhus, Rune Enger

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2018. 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
3.6field-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

41 citing papers in PubMed, 81 citations in OpenAlex.

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  10. Organellular imagingbioRxiv : the preprint server for biology · 2024
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  20. Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023
    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

10 authors at 3 institutions in 2 countries.

Kjell HeuserDepartment of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Cecilie G NomeInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Klas H PettersenLetten Centre and GliaLab, Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Knut S ÅbjørsbråtenLetten Centre and GliaLab, Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Vidar JensenLetten Centre and GliaLab, Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Wannan TangLetten Centre and GliaLab, Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Rolf SprengelMax Planck Research Group "Molecular Neurobiology" at the Institute for Anatomy and Cell Biology, Heidelberg University, Heidelberg, Germany.
Erik TaubøllDepartment of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Erlend A NagelhusDepartment of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Rune EngerDepartment of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
University of Oslo · NOOslo University Hospital · NOHeidelberg University · DE

Funding

SODIUM CHANNEL DIVERSITY IN THE DORSAL ROOT GANGLIONF32NS009021 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI MOSS, BRENDA LYNN · 1991 to 1994
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NINDS NIH HHS F32 NS009021
6 · The paper itself

Abstract

Epileptic seizures are associated with increased astrocytic Ca2+ signaling, but the fine spatiotemporal kinetics of the ictal astrocyte-neuron interplay remains elusive. By using 2-photon imaging of awake head-fixed mice with chronic hippocampal windows we demonstrate that astrocytic Ca2+ signals precede neuronal Ca2+ elevations during the initial bout of kainate-induced seizures. On average, astrocytic Ca2+ elevations preceded neuronal activity in CA1 by about 8 s. In subsequent bouts of epileptic seizures, astrocytes and neurons were activated simultaneously. The initial astrocytic Ca2+ elevation was abolished in mice lacking the type 2 inositol-1,4,5-trisphosphate-receptor (Itpr2-/-). Furthermore, we found that Itpr2-/- mice exhibited 60% less epileptiform activity compared with wild-type mice when assessed by telemetric EEG monitoring. In both genotypes we also demonstrate that spreading depression waves may play a part in seizure termination. Our findings imply a role for astrocytic Ca2+ signals in ictogenesis.

Indexed as

Calcium SignalingAnimalsAstrocytesEpilepsyExcitatory Amino Acid AgonistsHippocampusInositol 1,4,5-Trisphosphate ReceptorsKainic AcidMaleMice, Inbred C57BLMice, KnockoutNeuronsSeizuresExcitatory Amino Acid AgonistsInositol 1,4,5-Trisphosphate ReceptorsIp3r2 protein, mouseKainic Acid

Identifiers

PMID30169757
PMCPMC6188565
OpenAlexW2889292974

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.