Evidence map›Paper›PMID 29703263›Full record

ArticleVirology journal2018

Zika virus-induced hyper excitation precedes death of mouse primary neuron.

Julie Gaburro, Asim Bhatti, Vinod Sundaramoorthy, Megan Dearnley, Diane Green, Saeid Nahavandi, Prasad N Paradkar, Jean-Bernard Duchemin

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

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  14. Zika Virus Infection in the Developing Mouse Produces Dramatically Different Neuropathology Dependent on Viral Strain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  15. Article
  16. Transcriptomic Analysis ofInternational journal of molecular sciences · 2019
    Article
  17. Genome-wide CRISPR screen for Zika virus resistance in human neural cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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 2 institutions in 1 country.

Julie GaburroCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia.
Asim BhattiInstitute for Intelligent Systems Research and Innovation (IISRI), Deakin University, Geelong, Australia.
Vinod SundaramoorthyCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia.
Megan DearnleyCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia.
Diane GreenCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia.
Saeid NahavandiInstitute for Intelligent Systems Research and Innovation (IISRI), Deakin University, Geelong, Australia.
Prasad N ParadkarCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia.
Jean-Bernard DucheminCSIRO Health and Biosecurity, Australian Animal Health Laboratory, Geelong, Australia. Jean-Bernard.Duchemin@csiro.au.ORCID 0000-0001-5044-4855
Australian Centre for Disease Preparedness · AUDeakin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundZika virus infection in new born is linked to congenital syndromes, especially microcephaly. Studies have shown that these neuropathies are the result of significant death of neuronal progenitor cells in the central nervous system of the embryo, targeted by the virus. Although cell death via apoptosis is well acknowledged, little is known about possible pathogenic cellular mechanisms triggering cell death in neurons.

methodsWe used in vitro embryonic mouse primary neuron cultures to study possible upstream cellular mechanisms of cell death. Neuronal networks were grown on microelectrode array and electrical activity was recorded at different times post Zika virus infection. In addition to this method, we used confocal microscopy and Q-PCR techniques to observe morphological and molecular changes after infection.

resultsZika virus infection of mouse primary neurons triggers an early spiking excitation of neuron cultures, followed by dramatic loss of this activity. Using NMDA receptor antagonist, we show that this excitotoxicity mechanism, likely via glutamate, could also contribute to the observed nervous system defects in human embryos and could open new perspective regarding the causes of adult neuropathies.

conclusionsThis model of excitotoxicity, in the context of neurotropic virus infection, highlights the significance of neuronal activity recording with microelectrode array and possibility of more than one lethal mechanism after Zika virus infection in the nervous system.

Indexed as

Cell DeathAction PotentialsAnimalsBrainCells, CulturedGlutamic AcidMiceMice, Inbred C57BLModels, NeurologicalNerve NetNeuronsReceptors, N-Methyl-D-AspartateSignal TransductionSynaptic TransmissionVirus ReplicationZika VirusGlutamic AcidReceptors, N-Methyl-D-AspartateExcitotoxicityGlutamateHyper excitationMicroelectrode arrayPrimary neuronSpikeZika

Identifiers

PMID29703263
PMCPMC5922018
OpenAlexW2805786155

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.