Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17334
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dc.contributor.authorMcSweeney, K Melodi-
dc.contributor.authorGussow, Ayal B-
dc.contributor.authorBradrick, Shelton S-
dc.contributor.authorDugger, Sarah A-
dc.contributor.authorGelfman, Sahar-
dc.contributor.authorWang, Quanli-
dc.contributor.authorPetrovski, Slavé-
dc.contributor.authorFrankel, Wayne N-
dc.contributor.authorBoland, Michael J-
dc.contributor.authorGoldstein, David B-
dc.date2016-08-11-
dc.date.accessioned2018-04-03T04:55:59Z-
dc.date.available2018-04-03T04:55:59Z-
dc.date.issued2016-01-
dc.identifier.citationGenome research 2016; 26(10): 1411-1416-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17334-
dc.description.abstractCultured neuronal networks monitored with microelectrode arrays (MEAs) have been used widely to evaluate pharmaceutical compounds for potential neurotoxic effects. A newer application of MEAs has been in the development of in vitro models of neurological disease. Here, we directly evaluated the utility of MEAs to recapitulate in vivo phenotypes of mature microRNA-128 (miR-128) deficiency, which causes fatal seizures in mice. We show that inhibition of miR-128 results in significantly increased neuronal activity in cultured neuronal networks derived from primary mouse cortical neurons. These results support the utility of MEAs in developing in vitro models of neuroexcitability disorders, such as epilepsy, and further suggest that MEAs provide an effective tool for the rapid identification of microRNAs that promote seizures when dysregulated.-
dc.language.isoeng-
dc.titleInhibition of microRNA 128 promotes excitability of cultured cortical neuronal networks.-
dc.typeJournal Article-
dc.identifier.journaltitleGenome research-
dc.identifier.affiliationInstitute for Genomic Medicine, Columbia University Medical Center, New York, New York, USA-
dc.identifier.affiliationUniversity Program in Genetics and Genomics, Duke University, Durham, North Carolina, USA-
dc.identifier.affiliationComputational Biology and Bioinformatics, Duke University, Durham, North Carolina, USA-
dc.identifier.affiliationBiochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA-
dc.identifier.affiliationDepartment of Genetics and Development, Columbia University Medical Center, New York, New York, USA-
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia-
dc.identifier.affiliationDepartment of Neurology, Columbia University Medical Center, New York, New York, USA-
dc.identifier.affiliationDepartment of Medicine, Royal Melbourne Hospital, The University of Melbourne, Melbourne, Victoria, Australia-
dc.identifier.doi10.1101/gr.199828.115-
dc.identifier.orcid0000-0002-1527-961X-
dc.identifier.pubmedid27516621-
dc.type.austinJournal Article-
dc.type.austinResearch Support, Non-U.S. Gov't-
dc.type.austinResearch Support, N.I.H., Extramural-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
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