Evidence map›Paper›PMID 26484784›Full record

ReviewJournal of neuroscience methods2016

Models of drug-induced epileptiform synchronization in vitro.

Massimo Avoli, John G R Jefferys

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroscience methods, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  4. Modulation of CaScientific reports · 2024
    Article
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  9. The neurovasculature as a target in temporal lobe epilepsy.Brain pathology (Zurich, Switzerland) · 2023
    Review
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  17. Chronic Pharmacological Increase of Neuronal Activity Improves Sensory-Motor Dysfunction in Spinal Muscular Atrophy Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    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

2 authors at 2 institutions in 3 countries.

Massimo AvoliMontreal Neurological Institute and Departments of Neurology & Neurosurgery, and of Physiology, McGill University, Montréal, QC, Canada H3A 2B4; Department of Experimental Medicine, Facoltà di Medicina e Odontoiatria, Sapienza University of Rome, Roma 00185, Italy. Electronic address: massimo.avoli@mcgill.ca.
John G R JefferysDepartment of Pharmacology, University of Oxford, Oxford OX1 3QT, UK.
McGill University · CAUniversity of Oxford · GB

Funding

CIHR 74609CIHR 74609-2CIHR 8109CIHR 8109-6
6 · The paper itself

Abstract

Models of epileptiform activity in vitro have many advantages for recording and experimental manipulation. Neural tissues can be maintained in vitro for hours, and in neuronal or organotypic slice cultures for several weeks. A variety of drugs and other agents increase activity in these in vitro conditions, in many cases resulting in epileptiform activity, thus providing a direct model of symptomatic seizures. We review these preparations and the experimental manipulations used to induce epileptiform activity. The most common of drugs used are GABAA receptor antagonists and potassium channel blockers (notably 4-aminopyridine). Muscarinic agents also can induce epileptiform synchronization in vitro, and include potassium channel inhibition amongst their cellular actions. Manipulations of extracellular ions are reviewed in another paper in this special issue, as are ex vivo slices prepared from chronically epileptic animals and from people with epilepsy. More complex slices including extensive networks and/or several connected brain structures can provide insights into the dynamics of long range connections during epileptic activity. Visualization of slices also provides opportunities for identification of living neurons and for optical recording/stimulation and manipulation. Overall, the analysis of the epileptiform activity induced in brain tissue in vitro has played a major role in advancing our understanding of the cellular and network mechanisms of epileptiform synchronization, and it is expected to continue to do so in future.

Indexed as

Disease Models, AnimalGABA AntagonistsPotassium Channel BlockersAnimalsCells, CulturedCholinergic AgentsCortical SynchronizationEpilepsyHumansNerve NetOrgan Culture TechniquesCholinergic AgentsGABA AntagonistsPotassium Channel BlockersAnimal models in vitroEpileptiform synchronizationGABA(A) receptor antagonistsK(+) channel blockers

Identifiers

PMID26484784
PMCPMC4878885
OpenAlexW2185541914

What OpenQuestion holds

Textmetadata
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.