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|Title:||Cortical microarchitecture changes in genetic epilepsy.||Austin Authors:||Wimmer, Verena C;Li, Melody Y-S;Berkovic, Samuel F ;Petrou, Steven||Affiliation:||From The Florey Institute of Neuroscience and Mental Health (V.C.W., M.Y.-S.L., S.P.) and Centre for Neuroscience (S.P.), University of Melbourne; and Epilepsy Research Centre and Department of Medicine (S.F.B.), University of Melbourne, Austin Health, Australia||Issue Date:||4-Mar-2015||Publication information:||Neurology 2015; 84(13): 1308-16||Abstract:||The human GABAAγ2(R43Q) mutation is associated with genetic epilepsy. Because of the role of γ-aminobutyric acid (GABA) in brain development, we asked whether this epilepsy mutation might affect excitability by changing cortical cytoarchitecture.We used a mouse model harboring a heterozygous R43Q missense mutation in the GABAA receptor subunit γ2, as identified in a family with absence epilepsy and febrile seizures. Three-dimensional quantification of immunostained neurons (NeuN), inhibitory neurons (GABA), and inhibitory neuron subpopulations (calretinin, parvalbumin, and calbindin) was performed in fiducial somatosensory cortical columns of seizure-naive GABAAγ2(R43Q) and control mice.Of note, the densities of GABA-, calretinin-, parvalbumin-, and calbindin-containing neurons were increased, and somewhat perplexing, the ratio between putative excitatory and inhibitory neurons was decreased in GABAAγ2(R43Q) mice. Differences were detected in a layer-specific manner with greater overall effects in layers 2/3, 5, and 6, as compared with layers 1 and 4.Our results suggest that the γ2(R43Q) mutation significantly affects cortical microcircuitry in the cortex of this model of human genetic epilepsy.||Gov't Doc #:||25740860||URI:||http://ahro.austin.org.au/austinjspui/handle/1/12669||DOI:||10.1212/WNL.0000000000001415||URL:||https://pubmed.ncbi.nlm.nih.gov/25740860||Type:||Journal Article|
|Appears in Collections:||Journal articles|
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