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

Gaburro, Julie, Bhatti, Asim, Sundaramoorthy, Vinod, Dearnley, Megan, Green, Diane, Nahavandi, Saeid, Paradkar, Prasad N and Duchmin, Jean-Bernard 2018, Zika virus-induced hyper excitation precedes death of mouse primary neuron, Virology journal, vol. 15, pp. 1-13, doi: 10.1186/s12985-018-0989-4.

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Title Zika virus-induced hyper excitation precedes death of mouse primary neuron
Author(s) Gaburro, JulieORCID iD for Gaburro, Julie orcid.org/0000-0001-6609-6429
Bhatti, AsimORCID iD for Bhatti, Asim orcid.org/0000-0001-6876-1437
Sundaramoorthy, Vinod
Dearnley, Megan
Green, Diane
Nahavandi, SaeidORCID iD for Nahavandi, Saeid orcid.org/0000-0002-0360-5270
Paradkar, Prasad N
Duchmin, Jean-Bernard
Journal name Virology journal
Volume number 15
Article ID 79
Start page 1
End page 13
Total pages 13
Publisher BioMed Central
Place of publication London, Eng.
Publication date 2018-04-27
ISSN 1743-422X
Keyword(s) zika
primary neuron
microelectrode array
excitotoxicity
hyper excitation
spike
glutamate
science & technology
life sciences & biomedicine
virology
Summary Background
Zika 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.

Methods
We 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.

Results
Zika 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.

Conclusions
This 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.

Language eng
DOI 10.1186/s12985-018-0989-4
Field of Research 090303 Biomedical Instrumentation
090609 Signal Processing
100402 Medical Biotechnology Diagnostics (incl Biosensors)
110902 Cellular Nervous System
110804 Medical Virology
110999 Neurosciences not elsewhere classified
1108 Medical Microbiology
0605 Microbiology
Socio Economic Objective 970108 Expanding Knowledge in the Information and Computing Sciences
Copyright notice ©2018, The Authors
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30108126

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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.