Evidence map›Paper›PMID 27334140›Full record

ArticleJournal of neuroinflammation2016

Thalamocortical-auditory network alterations following cuprizone-induced demyelination.

Nikoo Ghaffarian, Masoud Mesgari, Manuela Cerina, Kerstin Göbel, Thomas Budde, Erwin-Josef Speckmann, Sven G Meuth, Ali Gorji

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Nikoo GhaffarianEpilepsy Research Center, Westfälische Wilhelms-Universität Münster, University of Münster, Robert-Koch-Straße 27a, 48149, Münster, Germany.
Masoud MesgariEpilepsy Research Center, Westfälische Wilhelms-Universität Münster, University of Münster, Robert-Koch-Straße 27a, 48149, Münster, Germany.
Manuela CerinaDepartment of Neurology, Westfälische Wilhelms-Universität, University of Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Kerstin GöbelDepartment of Neurology, Westfälische Wilhelms-Universität, University of Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany.
Thomas BuddeInstitute of Physiology I, Westfälische Wilhelms-Universität, Münster, Germany.
Erwin-Josef SpeckmannEpilepsy Research Center, Westfälische Wilhelms-Universität Münster, University of Münster, Robert-Koch-Straße 27a, 48149, Münster, Germany.
Sven G MeuthDepartment of Neurology, Westfälische Wilhelms-Universität, University of Münster, Albert-Schweitzer-Campus 1, Building A1, 48149, Münster, Germany. sven.meuth@ukmuenster.de.
Ali GorjiEpilepsy Research Center, Westfälische Wilhelms-Universität Münster, University of Münster, Robert-Koch-Straße 27a, 48149, Münster, Germany. gorjial@uni-muenster.de.
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDemyelination and remyelination are common pathological processes in many neurological disorders, including multiple sclerosis (MS). Clinical evidence suggests extensive involvement of the thalamocortical (TC) system in patients suffering from MS.

methodsUsing murine brain slices of the primary auditory cortex, we investigated the functional consequences of cuprizone-induced de- and remyelination on neuronal activity and auditory TC synaptic transmission in vitro.

resultsOur results revealed an impact of myelin loss and restoration on intrinsic cellular firing patterns, synaptic transmission, and neuronal plasticity in layer 3 and 4 neurons of the auditory TC network. While there was a complex hyper- and depolarizing shift of the resting membrane potential, spontaneous and induced action potential firing was reduced during demyelination and early remyelination. In addition, excitatory postsynaptic potential amplitudes were decreased and induction of LTP was reduced during demyelination.

conclusionsThese data indicate that demyelination-induced impairment of neurons and network activity within the TC system may underlie clinical symptoms observed in demyelinating diseases, corroborating human findings that disease progression is significantly correlated with microstructural tissue damage of the TC system. Further investigation into focal inflammation-induced demyelination models ex vivo and in vivo are needed to understand the functional implication of local and remote lesion formation on TC network activity in MS.

Indexed as

Action PotentialsAnimalsAuditory CortexAuditory PathwaysBiophysicsCuprizoneDemyelinating DiseasesDisease Models, AnimalElectric StimulationIn Vitro TechniquesMiceMice, Inbred C57BLMonoamine Oxidase InhibitorsMyelin Proteolipid ProteinNeuronsPatch-Clamp TechniquesCuprizoneMonoamine Oxidase InhibitorsMyelin Proteolipid ProteinAuditory cortexInternal capsuleLong-term potentiationNeuronal activity

Identifiers

PMID27334140
PMCPMC4918138
OpenAlexW2472120047

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.