Giant ankyrin-G stabilizes somatodendritic GABAergic synapses through opposing endocytosis of GABAA receptors

Wei Chou Tseng, Paul M. Jenkins, Masashi Tanaka, Richard Mooney, Vann Bennett*

*この研究の対応する著者

研究成果: Article査読

47 被引用数 (Scopus)

抄録

GABAA-receptor-based interneuron circuitry is essential for higher order function of the human nervous system and is implicated in schizophrenia, depression, anxiety disorders, and autism. Here we demonstrate that giant ankyrin-G (480-kDa ankyrin-G) promotes stability of somatodendritic GABAergic synapses in vitro and in vivo. Moreover, giant ankyrin-G forms developmentally regulated and cell-type-specific micron-scale domains within extrasynaptic somatodendritic plasma membranes of pyramidal neurons. We further find that giant ankyrin-G promotes GABAergic synapse stability through opposing endocytosis of GABAA receptors, and requires a newly described interaction with GABARAP, a GABAA receptor-associated protein. We thus present a new mechanism for stabilization of GABAergic interneuron synapses and micron-scale organization of extrasynaptic membrane that provides a rationale for studies linking ankyrin-G genetic variation with psychiatric disease and abnormal neurodevelopment.

本文言語English
ページ(範囲)1214-1219
ページ数6
ジャーナルProceedings of the National Academy of Sciences of the United States of America
112
4
DOI
出版ステータスPublished - 2015 1 27
外部発表はい

ASJC Scopus subject areas

  • 一般

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