Evidence map›Paper›PMID 27444269›Full record

ArticleScientific reports2016

Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism.

Alberto E Musto, Robert F Rosencrans, Chelsey P Walker, Surjyadipta Bhattacharjee, Chittalsinh M Raulji, Ludmila Belayev, Zhide Fang, William C Gordon, Nicolas G Bazan

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.0field-weighted citation impact, top 26% 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, 52 citations in OpenAlex.

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  8. The role of dendritic spines in epileptogenesis.Frontiers in cellular neuroscience · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Alberto E MustoNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Robert F RosencransNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Chelsey P WalkerNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Surjyadipta BhattacharjeeNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Chittalsinh M RauljiNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Ludmila BelayevNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Zhide FangBiostatistics, School of Public Health, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
William C GordonNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Nicolas G BazanNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA.
Louisiana State University Health Sciences Center New Orleans · US

Funding

Multiphoton ConfocalP30GM103340 · NIGMS · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2012 to 2016
$5.1M
NIGMS NIH HHS P30 GM103340
6 · The paper itself

Abstract

Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases in LE and that PAF receptor (PAF-r) ablation mitigates its progression. Synthetic PAF-r antagonists, when administered intraperitoneally in LE, re-establish hippocampal dendritic spine density and prevent formation of dysmorphic dendritic spines. Concomitantly, hippocampal interictal spikes, aberrant oscillations, and neuronal hyper-excitability, evaluated 15-16 weeks after LE using multi-array silicon probe electrodes implanted in the dorsal hippocampus, are reduced in PAF-r antagonist-treated mice. We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.

Indexed as

AnimalsBlood PlateletsDendritic SpinesDisease Models, AnimalEpilepsy, Temporal LobeHippocampusHumansLimbic LobeMiceNeuronal PlasticityNeuronsPlatelet Activating FactorPlatelet Membrane GlycoproteinsReceptors, G-Protein-CoupledPlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsReceptors, G-Protein-Coupled

Identifiers

PMID27444269
PMCPMC4957208
OpenAlexW2495437956

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.