Evidence map›Paper›PMID 35305155›Full record

ArticleCellular and molecular life sciences : CMLS2022

Controlling absence seizures from the cerebellar nuclei via activation of the G

Jan Claudius Schwitalla, Johanna Pakusch, Brix Mücher, Alexander Brückner, Dominic Alexej Depke, Thomas Fenzl, Chris I De Zeeuw, Lieke Kros, Freek E Hoebeek, Melanie D Mark

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Antiseizure Networks.Epilepsy currents · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
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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.

Jan Claudius SchwitallaDepartment of Behavioral Neuroscience, Ruhr-University Bochum, 44801, Bochum, Germany.
Johanna PakuschDepartment of Behavioral Neuroscience, Ruhr-University Bochum, 44801, Bochum, Germany.
Brix MücherDepartment of Zoology and Neurobiology, Ruhr-University Bochum, 44801, Bochum, Germany.
Alexander BrücknerInstitute of Physiology I, Medical Faculty, University of Bonn, 53127, Bonn, Germany.
Dominic Alexej DepkeEuropean Institute of Molecular Imaging, University of Münster, 48149, Münster, Germany.
Thomas FenzlDepartment of Anesthesiology and Intensive Care, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.
Chris I De ZeeuwDepartment of Neuroscience, Erasmus MC, 3015 AA, Rotterdam, The Netherlands.
Lieke KrosDepartment of Neuroscience, Erasmus MC, 3015 AA, Rotterdam, The Netherlands.
Freek E HoebeekDepartment for Developmental Origins of Disease, Wilhelmina Children's Hospital and Brain Center, University Medical Center Utrecht, 3584 EA, Utrecht, The Netherlands.
Melanie D MarkDepartment of Behavioral Neuroscience, Ruhr-University Bochum, 44801, Bochum, Germany. melanie.mark@rub.de.ORCID http://orcid.org/0000-0002-2788-6003

Funding

Deutsche Forschungsgemeinschaft 316803389Deutsche Forschungsgemeinschaft MA 5806/1-2Deutsche Forschungsgemeinschaft MA 5806/2-1
6 · The paper itself

Abstract

Absence seizures (ASs) are characterized by pathological electrographic oscillations in the cerebral cortex and thalamus, which are called spike-and-wave discharges (SWDs). Subcortical structures, such as the cerebellum, may well contribute to the emergence of ASs, but the cellular and molecular underpinnings remain poorly understood. Here we show that the genetic ablation of P/Q-type calcium channels in cerebellar granule cells (quirky) or Purkinje cells (purky) leads to recurrent SWDs with the purky model showing the more severe phenotype. The quirky mouse model showed irregular action potential firing of their cerebellar nuclei (CN) neurons as well as rhythmic firing during the wave of their SWDs. The purky model also showed irregular CN firing, in addition to a reduced firing rate and rhythmicity during the spike of the SWDs. In both models, the incidence of SWDs could be decreased by increasing CN activity via activation of the G

Indexed as

Cerebellar NucleiEpilepsy, AbsenceAction PotentialsAnimalsMiceSeizuresSignal TransductionAbsence epilepsyChemogenetic stimulationGPCRmGluR1Optogenetic stimulation

Identifiers

PMID35305155
PMCPMC8934336

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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.