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Title: Inhibition of microRNA 128 promotes excitability of cultured cortical neuronal networks.
Austin Authors: McSweeney, K Melodi;Gussow, Ayal B;Bradrick, Shelton S;Dugger, Sarah A;Gelfman, Sahar;Wang, Quanli;Petrovski, Slavé;Frankel, Wayne N;Boland, Michael J;Goldstein, David B
Affiliation: Institute for Genomic Medicine, Columbia University Medical Center, New York, New York, USA
University Program in Genetics and Genomics, Duke University, Durham, North Carolina, USA
Computational Biology and Bioinformatics, Duke University, Durham, North Carolina, USA
Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA
Department of Genetics and Development, Columbia University Medical Center, New York, New York, USA
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Neurology, Columbia University Medical Center, New York, New York, USA
Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Melbourne, Victoria, Australia
Issue Date: Jan-2016
Date: 2016-08-11
Publication information: Genome research 2016; 26(10): 1411-1416
Abstract: Cultured 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.
DOI: 10.1101/gr.199828.115
ORCID: 0000-0002-1527-961X
Journal: Genome research
PubMed URL: 27516621
Type: Journal Article
Appears in Collections:Journal articles

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