Evidence map›Paper›PMID 28154762›Full record

ArticleNeural plasticity2017

Pilocarpine-Induced Status Epilepticus Is Associated with Changes in the Actin-Modulating Protein Synaptopodin and Alterations in Long-Term Potentiation in the Mouse Hippocampus.

Maximilian Lenz, Marina Ben Shimon, Thomas Deller, Andreas Vlachos, Nicola Maggio

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  10. [Chronic phosphoproteomic in temporal lobe epilepsy mouse models induced by kainic acid].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2019
    Article
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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

5 authors at 3 institutions in 2 countries.

Maximilian LenzDepartment of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel; Institute of Anatomy II, Faculty of Medicine, Heinrich-Heine University, Düsseldorf, Germany; Institute of Clinical Neuroanatomy, Neuroscience Center Frankfurt, Goethe University, Frankfurt, Germany.
Marina Ben ShimonDepartment of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Thomas DellerInstitute of Clinical Neuroanatomy, Neuroscience Center Frankfurt, Goethe University, Frankfurt, Germany.
Andreas VlachosInstitute of Anatomy II, Faculty of Medicine, Heinrich-Heine University, Düsseldorf, Germany.ORCID 0000-0002-2646-3770
Nicola MaggioDepartment of Neurology, The Chaim Sheba Medical Center, Tel HaShomer, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Talpiot Medical Leadership Program, The Chaim Sheba Medical Center, Tel HaShomer, Israel; Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0001-9632-3338
Goethe University Frankfurt · DETel Aviv University · ILHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a complex neurological disorder which can severely affect neuronal function. Some patients may experience status epilepticus, a life-threatening state of ongoing seizure activity associated with postictal cognitive dysfunction. However, the molecular mechanisms by which status epilepticus influences brain function beyond seizure activity remain not well understood. Here, we addressed the question of whether pilocarpine-induced status epilepticus affects synaptopodin (SP), an actin-binding protein, which regulates the ability of neurons to express synaptic plasticity. This makes SP an interesting marker for epilepsy-associated alterations in synaptic function. Indeed, single dose intraperitoneal pilocarpine injection (250 mg/kg) in three-month-old male C57BL/6J mice leads to a rapid reduction in hippocampal SP-cluster sizes and numbers (in CA1 stratum radiatum of the dorsal hippocampus; 90 min after injection). In line with this observation (and previous work using SP-deficient mice), a defect in the ability to induce long-term potentiation (LTP) of Schaffer collateral-CA1 synapses is observed. Based on these findings we propose that status epilepticus could exert its aftereffects on cognition at least in part by perturbing SP-dependent mechanisms of synaptic plasticity.

Indexed as

ActinsAnimalsCytoskeletal ProteinsHippocampusLong-Term PotentiationMaleMiceMice, Inbred C57BLMicrofilament ProteinsPilocarpineStatus Epilepticusactin-modulating proteinsActinsCytoskeletal ProteinsMicrofilament ProteinsPilocarpineSynpo protein, mouse

Identifiers

PMID28154762
PMCPMC5244022
OpenAlexW2571443808

What OpenQuestion holds

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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.