Decreased Tonic Inhibition in Cerebellar Granule Cells Causes Motor Dysfunction in a Mouse Model of Angelman Syndrome-Reference-Cited by-同舟云学术

Decreased Tonic Inhibition in Cerebellar Granule Cells Causes Motor Dysfunction in a Mouse Model of Angelman Syndrome

Published:2012-12-05 Issue:163 Volume:4 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Egawa Kiyoshi¹,Kitagawa Kyoko²,Inoue Koichi¹,Takayama Masakazu¹,Takayama Chitoshi³,Saitoh Shinji⁴,Kishino Tatsuya⁵,Kitagawa Masatoshi²,Fukuda Atsuo¹

Affiliation:

1. Department of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan.

2. Department of Molecular Biology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan.

3. Department of Molecular Anatomy, School of Medicine, University of the Ryukyus, Nishihara 903-0215, Japan.

4. Department of Pediatrics and Neonatology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan.

5. Nagasaki University Center for Frontier Life Sciences, Nagasaki 852-8523, Japan.

Abstract

Ube3a deficiency causes a decrease in cerebellar tonic inhibition by preventing degradation of GABA transporter 1 in a mouse model of Angelman syndrome.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference63 articles.

1. Imprinted expression of the murine Angelman syndrome gene, Ube3a, in hippocampal and Purkinje neurons

2. Mutation of the Angelman Ubiquitin Ligase in Mice Causes Increased Cytoplasmic p53 and Deficits of Contextual Learning and Long-Term Potentiation

3. UBE3A/E6-AP mutations cause Angelman syndrome

4. Angelman syndrome: Consensus for diagnostic criteria

5. Derangements of Hippocampal Calcium/Calmodulin-Dependent Protein Kinase II in a Mouse Model for Angelman Mental Retardation Syndrome

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