|Title:||Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function.|
|Authors:||Kakizawa, Sho https://orcid.org/0000-0001-8396-5411 (unconfirmed)|
|Author's alias:||柿澤, 昌|
|Publisher:||Nature Publishing Group|
|Journal title:||The EMBO journal|
|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|
This is not the published version. Please cite only the published version.
|Appears in Collections:||Journal Articles|
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