NDLI: Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.

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Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.

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Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gallagher, Martin J. Zhou, Chengwen Deel, M. Elizabeth Arain, Fazal M. Flanagan, Christopher D. Patel, Ronak S. Murray, Clark R. Ding, Li Huang, Zhiling
Description	Author Affiliation: Zhou C ( Department of Neurology, Vanderbilt University, Nashville, Tennessee 37232, USA.)
Abstract	Patients with generalized epilepsy exhibit cerebral cortical disinhibition. Likewise, mutations in the inhibitory ligand-gated ion channels, GABAA receptors (GABAARs), cause generalized epilepsy syndromes in humans. Recently, we demonstrated that heterozygous knock-out (Het 1KO) of the human epilepsy gene, the GABAAR 1 subunit, produced absence epilepsy in mice. Here, we determined the effects of Het 1KO on the expression and physiology of GABAARs in the mouse cortex. We found that Het 1KO caused modest reductions in the total and surface expression of the ß2 subunit but did not alter ß1 or ß3 subunit expression, results consistent with a small reduction of GABAARs. Cortices partially compensated for Het 1KO by increasing the fraction of residual 1 subunit on the cell surface and by increasing total and surface expression of 3, but not 2, subunits. Co-immunoprecipitation experiments revealed that Het 1KO increased the fraction of 1 subunits, and decreased the fraction of 3 subunits, that associated in hybrid 1 3ßÎ³ receptors. Patch clamp electrophysiology studies showed that Het 1KO layer VI cortical neurons exhibited reduced inhibitory postsynaptic current peak amplitudes, prolonged current rise and decay times, and altered responses to benzodiazepine agonists. Finally, application of inhibitors of dynamin-mediated endocytosis revealed that Het 1KO reduced base-line GABAAR endocytosis, an effect that probably contributes to the observed changes in GABAAR expression. These findings demonstrate that Het 1KO exerts two principle disinhibitory effects on cortical GABAAR-mediated inhibitory neurotransmission: 1) a modest reduction of GABAAR number and 2) a partial compensation with GABAAR isoforms that possess physiological properties different from those of the otherwise predominant 1ßÎ³ GABAARs.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	29
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-07-19
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cerebral Cortex Metabolism Endocytosis Epilepsy, Absence Genetics Physiopathology Alleles Animals Benzodiazepines Pharmacology COS Cells Cell Membrane Drug Effects Cercopithecus Aethiops Disease Models, Animal Dynamins Endoplasmic Reticulum Pathology GABA-A Receptor Agonists Gene Expression Regulation Heterozygote Kinetics Mice Mice, Knockout Models, Biological Protein Binding Protein Subunits RNA, Messenger Receptors, GABA-A Synapses Gamma-Aminobutyric Acid Research Support, N.I.H., Extramural Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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