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. Attached Files Name Description MIMEType Size Downloads bhatti-zikavirusinduced-2018.pdf Published version application/pdf 10.15MB 5 Title Zika virus-induced hyper excitation precedes death of mouse primary neuron Author(s) Gaburro, Julie orcid.org/0000-0001-6609-6429 Bhatti, Asim orcid.org/0000-0001-6876-1437 Sundaramoorthy, Vinod Dearnley, Megan Green, Diane 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 Persistent URL http://hdl.handle.net/10536/DRO/DU:30108126 Document type: Journal Article Collections: Centre for Intelligent Systems Research Open Access Collection Elements - New records (hidden) Related Links Link Description Connect to published version (open access) Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. 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. Versions Version Filter Type Fri, 04 May 2018, 10:41:56 EST Sat, 05 May 2018, 05:00:38 EST Mon, 07 May 2018, 08:28:10 EST Sat, 19 May 2018, 02:33:50 EST Sat, 26 May 2018, 02:30:43 EST Wed, 26 Sep 2018, 15:41:06 EST Wed, 26 Sep 2018, 15:43:34 EST Wed, 26 Sep 2018, 15:44:22 EST Wed, 26 Sep 2018, 15:54:48 EST Filtered Full Citation counts:   Cited 0 times in TR Web of Science Cited 0 times in Scopus Search Google Scholar Access Statistics: 8 Abstract Views, 7 File Downloads  -  Detailed Statistics Created: Fri, 04 May 2018, 10:41:56 EST

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.