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:https://doi.org/10.1083/jcb.131.6.1789

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タイトル	Synapsin I Deficiency Results in the Structural Change in the Presynaptic Terminals in the Murine Nervous System
著者	NRID 1000020272487 1000020272487 著者名 Takei, Yosuke
	NRID 1000040251441 1000040251441 著者名 Harada, Akihiro
	NRID 1000020272429 1000020272429 著者名 Takeda, Sen
	NRID 1000010322041 1000010322041 著者名 Kobayashi, Katsunori
	NRID 1000000262022 1000000262022 著者名 Terada, Sumio
	NRID 1000010183550 1000010183550 著者名 Noda, Tetsuo
	NRID 1000040092415 1000040092415 著者名 Takahashi, Tomoyuki
	NRID 1000020010085 1000020010085 著者名 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.
出版者	The Rockefeller University Press
収録物名	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
言語	英語
ハンドルURL	https://hdl.handle.net/11094/23087
ISSN	00219525
NCID	AA00694812
関連情報 (isIdenticalTo)	DOI (出版社版) https://doi.org/10.1083/jcb.131.6.1789
アクセス権	open access
出版タイプ	Version of Record
カテゴリ	学術雑誌論文 Journal Article

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
DC.type' scheme='DCTERMS.DCMIType	text
DCTERMS.issued' scheme='DCTERMS.W3CDTF	1995-11-15
DC.identifier	https://doi.org/10.1083/jcb.131.6.1789
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.
DC.format	application/pdf
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	https://doi.org/10.1083/jcb.131.6.1789
citation_public_url	https://hdl.handle.net/11094/23087

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