Evidence map›Paper›PMID 26909803›Full record

ArticlePloS one2016

A Low Mortality, High Morbidity Reduced Intensity Status Epilepticus (RISE) Model of Epilepsy and Epileptogenesis in the Rat.

Tamara Modebadze, Nicola H Morgan, Isabelle A A Pérès, Rebecca D Hadid, Naoki Amada, Charlotte Hill, Claire Williams, Ian M Stanford, Christopher M Morris, Roland S G Jones and 2 more

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  4. Differential regulation of KExperimental animals · 2025
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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

12 authors.

Tamara ModebadzeAston Brain Centre, Aston University, School of Life and Health Sciences, Birmingham, United Kingdom.
Nicola H MorganAston Brain Centre, Aston University, School of Life and Health Sciences, Birmingham, United Kingdom.
Isabelle A A PérèsSchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Rebecca D HadidSchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Naoki AmadaSchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Charlotte HillSchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Claire WilliamsSchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Ian M StanfordAston Brain Centre, Aston University, School of Life and Health Sciences, Birmingham, United Kingdom.
Christopher M MorrisMedical Toxicology Centre, Newcastle University, Wolfson Building, Claremont Place, Newcastle upon Tyne, United Kingdom.
Roland S G JonesDepartment of Pharmacology, University of Bath, Claverton Down, Bath, United Kingdom.
Benjamin J WhalleySchool of Pharmacy, Hopkins Life Sciences Building, University of Reading, Whiteknights, Reading, Berkshire, United Kingdom.
Gavin L WoodhallAston Brain Centre, Aston University, School of Life and Health Sciences, Birmingham, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Animal models of acquired epilepsies aim to provide researchers with tools for use in understanding the processes underlying the acquisition, development and establishment of the disorder. Typically, following a systemic or local insult, vulnerable brain regions undergo a process leading to the development, over time, of spontaneous recurrent seizures. Many such models make use of a period of intense seizure activity or status epilepticus, and this may be associated with high mortality and/or global damage to large areas of the brain. These undesirable elements have driven improvements in the design of chronic epilepsy models, for example the lithium-pilocarpine epileptogenesis model. Here, we present an optimised model of chronic epilepsy that reduces mortality to 1% whilst retaining features of high epileptogenicity and development of spontaneous seizures. Using local field potential recordings from hippocampus in vitro as a probe, we show that the model does not result in significant loss of neuronal network function in area CA3 and, instead, subtle alterations in network dynamics appear during a process of epileptogenesis, which eventually leads to a chronic seizure state. The model's features of very low mortality and high morbidity in the absence of global neuronal damage offer the chance to explore the processes underlying epileptogenesis in detail, in a population of animals not defined by their resistance to seizures, whilst acknowledging and being driven by the 3Rs (Replacement, Refinement and Reduction of animal use in scientific procedures) principles.

Indexed as

Disease Models, AnimalAnimalsBehavior, AnimalDisease ProgressionHumansMaleMorbidityRatsRats, WistarRecurrenceStatus Epilepticus

Identifiers

PMID26909803
PMCPMC4765932

What OpenQuestion holds

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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.