Sodium-potassium ATPase emerges as a player in hippocampal phenotypes of Angelman syndrome mice
Author(s) -
Jada J. Hallengren,
Ryan J Vaden
Publication year - 2014
Publication title -
journal of neurophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.302
H-Index - 245
eISSN - 1522-1598
pISSN - 0022-3077
DOI - 10.1152/jn.00760.2013
Subject(s) - angelman syndrome , hippocampal formation , neuroscience , ataxia , long term potentiation , neurodevelopmental disorder , intellectual disability , psychology , hippocampus , chemistry , developmental psychology , biochemistry , psychiatry , autism , gene , receptor
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.
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