title: Sodium-potassium ATPase emerges as a player in hippocampal phenotypes of Angelman syndrome mice.
abstract: Angelman syndrome is a neurodevelopmental disorder characterized by intellectual disabilities, ataxia, and unusually happy affect. The hippocampal pyramidal cells of Angelman syndrome model mice have altered intrinsic membrane properties, which Kaphzan et al. (Cell Rep 4: 405-412, 2013) demonstrate can be corrected by genetic reduction of the α1-subunit of the sodium-potassium ATPase. Intriguingly, this manipulation also restores hippocampal long-term potentiation and learning. In this Neuro Forum, we discuss translational implications of this work and remaining questions left in its wake.
authors: Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama jjh85@uab.edu.
authors: Jada J
authors: JJ
authors: Hallengren
authors: Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama.
authors: Ryan J
authors: RJ
authors: Vaden
mesh_terms: D017204:Angelman Syndrome / Q000235:genetics* / Q000473:pathology*; D000818:Animals; D005260:Female; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics*
chemical_list: D000254:Sodium-Potassium-Exchanging ATPase
keywords: Angelman syndrome; intrinsic excitability; long-term potentiation; sodium-potassium ATPase