Evidence map›Paper›PMID 26709882›Full record

ArticleEpilepsy research2016

Widespread neuronal injury in a model of cholinergic status epilepticus in postnatal day 7 rat pups.

Daniel Torolira, Lucie Suchomelova, Claude G Wasterlain, Jerome Niquet

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Epilepsy research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.7field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Status Epilepticus in the Neonate: Updates in Treatment Strategies.Current treatment options in neurology · 2019
    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

4 authors at 1 institution in 1 country.

Daniel ToroliraEpilepsy Research Laboratory (151), Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Lucie SuchomelovaEpilepsy Research Laboratory (151), Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Claude G WasterlainEpilepsy Research Laboratory (151), Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA; Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA; Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Jerome NiquetEpilepsy Research Laboratory (151), Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA; Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. Electronic address: jniquet@ucla.edu.
VA Greater Los Angeles Healthcare System · US

Funding

Rational polytherapy in the treatment of cholinergic seizuresU01NS074926 · NINDS · BRENTWOOD BIOMEDICAL RESEARCH INSTITUTE · PI WASTERLAIN, CLAUDE G · 2011 to 2015
$3.3M
Treatment of Status Epilepticus: A Translational ProposalI01BX000273 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI WASTERLAIN, CLAUDE G · 2009 to 2017
–
BLRD VA I01 BX000273NINDS NIH HHS U01 NS074926NINDS NIH HHS UO1 NS074926
6 · The paper itself

Abstract

objectiveStatus Epilepticus (SE) is common in neonates and infants, and is associated with neuronal injury and adverse developmental outcomes. However, the role of SE in this injury is uncertain. Until now, we have lacked an animal model in which seizures result in neuronal injury in rodent models at ages below postnatal day 12 (P12) unless seizures are combined with inflammatory stressors.

methodsWe induced SE with high-dose lithium and pilocarpine in P7 rats, which are developmentally close to human neonates. Several EEG measures and O2 saturation were recorded during the 6h following initiation of SE. We assessed neuronal injury at 6 and 24h post-SE onset using Fluoro-Jade B staining (FJB) and caspase-3a immunoreactivity (IR).

resultsEEGs showed continuous polyspikes activity for 54.3 ± 6.7 min, while O2 saturation showed no significant hypoxemia. By 24h after SE onset, significant neuronal injury was observed in CA1/subiculum, CA3, dentate gyrus, thalamus, neocortex, amygdala, piriform cortex, lateral entorhinal cortex, hypothalamus, caudate putamen, globus pallidus, ventral pallidum, and nucleus accumbens. At 24h post-SE, caspase-3a IR was significantly increased in CA1/subiculum, thalamus, and neocortex compared to sham, and caspase-3a IR neurons had fragmented nuclei, suggesting that SE triggered an irreversible form of cell injury. SIGNIFICANCE: In conclusion, we have developed a model of cholinergic SE in P7 rat pups, which combines high survival (69.9% survival at 24h) and widespread brain injury. These studies suggest that the immature brain is vulnerable to severe forms of SE.

Indexed as

AnimalsAnimals, NewbornBrainCaspase 3Disease Models, AnimalElectrocorticographyElectroencephalographyFemaleImmunohistochemistryLithium CompoundsMaleNeuronsOxygenPilocarpineRats, Sprague-DawleyStatus EpilepticusCasp3 protein, ratCaspase 3Lithium CompoundsOxygenPilocarpineActive caspase-3Fluoro–Jade BHippocampusImmature brainNeonateSeizures

Identifiers

PMID26709882
PMCPMC4740206
OpenAlexW2176792429

What OpenQuestion holds

Textmetadata
LicenceTDM
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.