Format

Send to

Choose Destination
J Neurophysiol. 2014 Jul 1;112(1):5-8. doi: 10.1152/jn.00760.2013. Epub 2014 Feb 5.

Sodium-potassium ATPase emerges as a player in hippocampal phenotypes of Angelman syndrome mice.

Author information

1
Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama jjh85@uab.edu.
2
Department of Neurobiology and Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama.

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.

KEYWORDS:

Angelman syndrome; intrinsic excitability; long-term potentiation; sodium-potassium ATPase

PMID:
24501262
PMCID:
PMC4064391
DOI:
10.1152/jn.00760.2013
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center