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Title: Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function.
Authors: Kakizawa, Sho  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0001-8396-5411 (unconfirmed)
Yamazawa, Toshiko
Chen, Yili
Ito, Akihiro
Murayama, Takashi
Oyamada, Hideto
Kurebayashi, Nagomi
Sato, Osamu
Watanabe, Masahiko
Mori, Nozomu
Oguchi, Katsuji
Sakurai, Takashi
Takeshima, Hiroshi  kyouindb  KAKEN_id
Saito, Nobuhito
Iino, Masamitsu
Author's alias: 柿澤, 昌
Keywords: calcium
nitric oxide
ryanodine receptor
synapse
Issue Date: 18-Jan-2012
Publisher: Nature Publishing Group
Journal title: The EMBO journal
Volume: 31
Issue: 2
Start page: 417
End page: 428
Abstract: Mobilization of intracellular Ca(2+) stores regulates a multitude of cellular functions, but the role of intracellular Ca(2+) release via the ryanodine receptor (RyR) in the brain remains incompletely understood. We found that nitric oxide (NO) directly activates RyRs, which induce Ca(2+) release from intracellular stores of central neurons, and thereby promote prolonged Ca(2+) signalling in the brain. Reversible S-nitrosylation of type 1 RyR (RyR1) triggers this Ca(2+) release. NO-induced Ca(2+) release (NICR) is evoked by type 1 NO synthase-dependent NO production during neural firing, and is essential for cerebellar synaptic plasticity. NO production has also been implicated in pathological conditions including ischaemic brain injury, and our results suggest that NICR is involved in NO-induced neuronal cell death. These findings suggest that NICR via RyR1 plays a regulatory role in the physiological and pathophysiological functions of the brain.
Rights: © 2012 European Molecular Biology Organization
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/158743
DOI(Published Version): 10.1038/emboj.2011.386
PubMed ID: 22036948
Appears in Collections:Journal Articles

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