Evidence map›Paper›PMID 40932659›Full record

ArticleEpilepsia2026

Potassium-chloride cotransporter 2 activity dampens induced ictal-like activity in neocortical slices containing the seizure propagation zone of temporal lobe epilepsy patients.

Alice Falck, Janna Lehnhoff, Mahraz Behbood, Egor Byvaltcev, Annette Aigner, Helena Radbruch, Pawel Fidzinski, Jan-Hendrik Schleimer, Gabriel M S Janach, Noah Döhne and 7 more

Abstract read
In one paragraph

Article in Epilepsia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

17 authors.

Alice FalckCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0009-0005-5430-8953
Janna LehnhoffCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Mahraz BehboodDepartment of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-7047-4979
Egor ByvaltcevCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-3922-0233
Annette AignerInstitute of Biometry and Clinical Epidemiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0003-4891-8921
Helena RadbruchDepartment of Neuropathology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0001-6941-3397
Pawel FidzinskiDepartment of Neurology With Experimental Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0001-6373-4763
Jan-Hendrik SchleimerDepartment of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-2156-330X
Gabriel M S JanachCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0001-6844-2698
Noah DöhneCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0009-0002-6322-7555
Julia OnkenDepartment of Neurosurgery, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-2859-4395
Thilo KalbhennDepartment of Neurosurgery, Evangelisches Klinikum Bethel, Universitätsklinikum OWL der Universität Bielefeld, Bielefeld, Germany.ORCID https://orcid.org/0000-0001-6249-629X
Thomas SauvignyDepartment of Neurosurgery, Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-8363-9576
Rudolf A DeiszCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Susanne SchreiberDepartment of Biology, Institute for Theoretical Biology, Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0003-3913-5650
Martin HoltkampDepartment of Neurology With Experimental Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0003-2258-1670
Ulf StraussCenter for Anatomy, Institute for Cell Biology and Neurobiology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-1534-6624

Funding

Deutsche Forschungsgemeinschaft DFG DE 419/9-1 | STR 865/5-1Einstein Stiftung Berlin EP-2021-621European Research Council 864243
6 · The paper itself

Abstract

objectiveThe K

methodsWe induced network activity in postoperative acute neocortical brain slices from humans with temporal lobe epilepsy under low Mg

resultsModulation of KCC2 activity altered the induced network activity; KCC2 block reversibly led to substantially increased activity, preferentially in and propagating through supragranular layers. Correspondingly, enhancing KCC2 activity reduced network activity there. Almost all individual supragranular pyramidal neurons tested had functional KCC2, that is, certain Cl SIGNIFICANCE: Our data show that KCC2 mitigates ictal-like activity in the seizure propagation zone of human neocortex, thereby further promoting KCC2 as a therapeutic target.

Indexed as

Epilepsy, Temporal LobeNeocortexSeizuresSymportersAdultFemaleHumansK Cl- CotransportersMaleMiddle AgedPatch-Clamp TechniquesPyramidal CellsK Cl- CotransportersSymporterschloride homeostasisKCC2layer 2/3microelectrode Arrayseizure propagation

Identifiers

PMID40932659
PMCPMC12893269

What OpenQuestion holds

Textmetadata
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.