Synapsin I Deficiency Results in the Structural Change in the Presynaptic Terminals in the Murine Nervous System

Takei, Yosuke; Harada, Akihiro; Takeda, Sen; Kobayashi, Katsunori; Terada, Sumio; Noda, Tetsuo; Takahashi, Tomoyuki; Hirokawa, Nobutaka

doi:info:doi/10.1083/jcb.131.6.1789

このアイテムのアクセス数:129件（2020-10-20 12:13 集計）

このアイテムへのリンクには次のURLをご利用ください:https://doi.org/10.1083/jcb.131.6.1789

このアイテムへのリンクには次のURLをご利用ください:http://hdl.handle.net/11094/23087

閲覧可能ファイル

ファイル	フォーマット	サイズ	閲覧回数	説明
jcb_131_6_1789	pdf	5.61 MB	226

論文情報

タイトル	Synapsin I Deficiency Results in the Structural Change in the Presynaptic Terminals in the Murine Nervous System
著者	Takei, Yosuke Takei, Yosuke
	Harada, Akihiro Harada, Akihiro
	Takeda, Sen Takeda, Sen
	Kobayashi, Katsunori Kobayashi, Katsunori
	Terada, Sumio Terada, Sumio
	Noda, Tetsuo Noda, Tetsuo
	Takahashi, Tomoyuki Takahashi, Tomoyuki
	Hirokawa, Nobutaka Hirokawa, Nobutaka
抄録	Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure.
公開者	The Rockefeller University Press
掲載誌名	Journal of Cell Biology
巻	131
号	6
開始ページ	1789
終了ページ	1800
刊行年月	1995-11-15
ISSN	00219525
NCID	AA00694812
DOI	info:doi/10.1083/jcb.131.6.1789
URL	http://hdl.handle.net/11094/23087
言語	英語
カテゴリ	学術雑誌論文 Journal Article

著者版フラグ	publisher
NII資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
dcmi資源タイプ	text
DCTERMS.bibliographicCitation	Journal of Cell Biology.131(6) P.1789-P.1800
DC.title	Synapsin I Deficiency Results in the Structural Change in the Presynaptic Terminals in the Murine Nervous System
DC.creator	Takei, Yosuke
	Harada, Akihiro
	Takeda, Sen
	Kobayashi, Katsunori
	Terada, Sumio
	Noda, Tetsuo
	Takahashi, Tomoyuki
	Hirokawa, Nobutaka
DC.publisher	The Rockefeller University Press
DC.language" scheme="DCTERMS.RFC1766	英語
DCTERMS.issued" scheme="DCTERMS.W3CDTF	1995-11-15
DC.identifier	info:doi/10.1083/jcb.131.6.1789
DC.identifier" scheme="DCTERMS.URI	http://hdl.handle.net/11094/23087
DCTERMS.abstract	Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure.
citation_title	Synapsin I Deficiency Results in the Structural Change in the Presynaptic Terminals in the Murine Nervous System
citation_author	Takei, Yosuke
	Harada, Akihiro
	Takeda, Sen
	Kobayashi, Katsunori
	Terada, Sumio
	Noda, Tetsuo
	Takahashi, Tomoyuki
	Hirokawa, Nobutaka
citation_publisher	The Rockefeller University Press
citation_language	英語
citation_date	1995-11-15
citation_journal_title	Journal of Cell Biology
citation_volume	131
citation_issue	6
citation_firstpage	1789
citation_lastpage	1800
citation_issn	00219525
citation_doi	info:doi/10.1083/jcb.131.6.1789
citation_public_url	http://hdl.handle.net/11094/23087

閲覧可能ファイル

論文情報

論文詳細を表示