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Nesfatin-1 evokes Ca2+ signaling in isolated vagal afferent neurons via Ca2+ influx through N-type channels

フォーマット:
論文
責任表示:
Iwasaki, Yusaku ; Nakabayashi, Hajime ; Kakei, Masafumi ; Shimizu, Hiroyuki ; Mori, Masatomo ; Yada, Toshihiko
言語:
英語
出版情報:
Elsevier, 2009-12-18
著者名:
Iwasaki, Yusaku
Nakabayashi, Hajime
Kakei, Masafumi
Shimizu, Hiroyuki
Mori, Masatomo
Yada, Toshihiko
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掲載情報:
Biochemical and Biophysical Research Communications
ISSN:
0006-291x  CiNii Research  Webcat Plus  JAIRO
巻:
390
通号:
3
開始ページ:
958
終了ページ:
962
バージョン:
author
概要:
金沢大学医薬保健研究域医学系<br />Nesfatin-1, processed from nucleobindin 2, is an anorexigenic peptide expressed in the brain and several peripheral tissues including the stomach and pancreas. Peripheral, as well as intracerebroventricular, admini stration of nesfatin-1 suppresses feeding behavior, though underlying mechanisms are unknown. In this study, we examined effects of nesfatin-1 on cytosolic Ca2+ concentration ([Ca2+]i) in the neurons isolated from the vagal afferent nodose ganglion of mice. Nesfatin-1 at 10-10-10-8 M increased [Ca2+]i in the isolated neurons in a concentration-dependent manner, and at 10-8 M it increased [Ca2+]i in 33 out of 263 (12.5%) neurons. These responses were inhibited under Ca2+-free conditions and by N-type Ca2+ channel blocker, ω-conotoxin GVIA. All the nesfatin-1-responsive neurons also exhibited [Ca2+]i responses to capsaicin and cholecystokinin-8. These results provide direct evidence that nesfatin-1 activates vagal afferent neurons by stimulating Ca2+ influx through N-type channels, demonstrating the machinery through which peripheral nesfatin-1 can convey signals to the brain. © 2009 Elsevier Inc. All rights reserved. 続きを見る
URL:
http://hdl.handle.net/2297/20509
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