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Title: Nitric oxide-induced calcium release: activation of type 1 ryanodine receptor by endogenous nitric oxide.
Authors: Kakizawa, Sho  kyouindb  KAKEN_id  orcid (unconfirmed)
Yamazawa, Toshiko
Iino, Masamitsu
Author's alias: 柿澤, 昌
Keywords: Purkinje cell
nitric oxide
ryanodine receptor
synaptic plasticity
Issue Date: 1-Jan-2013
Publisher: Landes Bioscience
Journal title: Channels
Volume: 7
Issue: 1
Start page: 1
End page: 5
Abstract: Ryanodine receptors (RyRs), located in the sarcoplasmic/endoplasmic reticulum (SR/ER) membrane, are required for intracellular Ca2+ release that is involved in a wide range of cellular functions. In addition to Ca2+-induced Ca2+ release in cardiac cells and voltage-induced Ca2+ release in skeletal muscle cells, we recently identified another mode of intracellular Ca2+ mobilization mediated by RyR, i.e., nitric oxide-induced Ca2+ release (NICR), in cerebellar Purkinje cells. NICR is evoked by neuronal activity, is dependent on S-nitrosylation of type 1 RyR (RyR1) and is involved in the induction of long-term potentiation (LTP) of cerebellar synapses. In this addendum, we examined whether peroxynitrite, which is produced by the reaction of nitric oxide with superoxide, may also have an effect on the Ca2+ release via RyR1 and the cerebellar LTP. We found that scavengers of peroxynitrite have no significant effect either on the Ca2+ release via RyR1 or on the cerebellar LTP. We also found that an application of a high concentration of peroxynitrite does not reproduce neuronal activity-dependent Ca2+ release in Purkinje cells. These results support that NICR is induced by endogenous nitric oxide produced by neuronal activity through S-nitrosylation of RyR1.
Rights: © 2013 Landes Bioscience
This is not the published version. Please cite only the published version.
DOI(Published Version): 10.4161/chan.22555
PubMed ID: 23247505
Appears in Collections:Journal Articles

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