Literature DB >> 24501262

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

Jada J Hallengren1, Ryan J Vaden2.   

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.
Copyright © 2014 the American Physiological Society.

Entities:  

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

Mesh:

Substances:

Year:  2014        PMID: 24501262      PMCID: PMC4064391          DOI: 10.1152/jn.00760.2013

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  31 in total

1.  Immunofluorescent localization of three Na,K-ATPase isozymes in the rat central nervous system: both neurons and glia can express more than one Na,K-ATPase.

Authors:  K M McGrail; J M Phillips; K J Sweadner
Journal:  J Neurosci       Date:  1991-02       Impact factor: 6.167

2.  Derangements of hippocampal calcium/calmodulin-dependent protein kinase II in a mouse model for Angelman mental retardation syndrome.

Authors:  Edwin J Weeber; Yong-Hui Jiang; Ype Elgersma; Andrew W Varga; Yarimar Carrasquillo; Sarah E Brown; Jill M Christian; Banefsheh Mirnikjoo; Alcino Silva; Arthur L Beaudet; J David Sweatt
Journal:  J Neurosci       Date:  2003-04-01       Impact factor: 6.167

3.  Ubiquitination of Na,K-ATPase alpha1 and alpha2 subunits.

Authors:  M V Coppi; G Guidotti
Journal:  FEBS Lett       Date:  1997-04-01       Impact factor: 4.124

4.  Changes in the mRNAs encoding voltage-gated sodium channel types II and III in human epileptic hippocampus.

Authors:  W R Whitaker; R L Faull; M Dragunow; E W Mee; P C Emson; J J Clare
Journal:  Neuroscience       Date:  2001       Impact factor: 3.590

5.  UBE3A/E6-AP mutations cause Angelman syndrome.

Authors:  T Kishino; M Lalande; J Wagstaff
Journal:  Nat Genet       Date:  1997-01       Impact factor: 38.330

6.  The Angelman syndrome candidate gene, UBE3A/E6-AP, is imprinted in brain.

Authors:  C Rougeulle; H Glatt; M Lalande
Journal:  Nat Genet       Date:  1997-09       Impact factor: 38.330

Review 7.  Angelman syndrome reviewed from a neurophysiological perspective. The UBE3A-GABRB3 hypothesis.

Authors:  B Dan; S G Boyd
Journal:  Neuropediatrics       Date:  2003-08       Impact factor: 1.947

8.  Mutation of the Angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation.

Authors:  Y H Jiang; D Armstrong; U Albrecht; C M Atkins; J L Noebels; G Eichele; J D Sweatt; A L Beaudet
Journal:  Neuron       Date:  1998-10       Impact factor: 17.173

9.  Mice lacking the beta3 subunit of the GABAA receptor have the epilepsy phenotype and many of the behavioral characteristics of Angelman syndrome.

Authors:  T M DeLorey; A Handforth; S G Anagnostaras; G E Homanics; B A Minassian; A Asatourian; M S Fanselow; A Delgado-Escueta; G D Ellison; R W Olsen
Journal:  J Neurosci       Date:  1998-10-15       Impact factor: 6.167

10.  Calcium/calmodulin-dependent protein kinase II contributes to activity-dependent filopodia growth and spine formation.

Authors:  Pascal Jourdain; Kohji Fukunaga; Dominique Muller
Journal:  J Neurosci       Date:  2003-11-19       Impact factor: 6.167

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