Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function
Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function
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DOI：
10.1038/emboj.2011.386
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发表时间：
2012-01-18
期刊：
影响因子：
11.4
通讯作者：
Iino, Masamitsu
中科院分区：
文献类型：
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作者：
Kakizawa, Sho;Yamazawa, Toshiko;Iino, Masamitsu
细胞内Ca 2+库的动员调节多种细胞功能，但是通过脑中的兰尼碱受体（RyR）的细胞内Ca 2+释放的作用仍然不完全清楚。我们发现，一氧化氮（NO）直接激活RyR，诱导Ca 2+从中枢神经元的细胞内储存释放，从而促进大脑中长时间的Ca 2+信号传导。1型RyR（RyR 1）的可逆S-亚硝基化触发这种Ca 2+释放。NO诱导的Ca 2+释放（NICR）是由神经放电过程中1型NO氧化酶依赖的NO产生引起的，并且对小脑突触可塑性至关重要。NO的产生也涉及病理条件，包括缺血性脑损伤，我们的研究结果表明，NICR参与NO诱导的神经元细胞死亡。这些发现表明，NICR通过RyR 1在大脑的生理和病理生理功能中起着调节作用。The EMBO Journal（2012）31，417-428. doi：10.1038/doj.2011.386; 2011年10月28日在线发布
Mobilization of intracellular Ca2+ stores regulates a multitude of cellular functions, but the role of intracellular Ca2+ release via the ryanodine receptor (RyR) in the brain remains incompletely understood. We found that nitric oxide (NO) directly activates RyRs, which induce Ca2+ release from intracellular stores of central neurons, and thereby promote prolonged Ca2+ signalling in the brain. Reversible S-nitrosylation of type 1 RyR (RyR1) triggers this Ca2+ release. NO-induced Ca2+ 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. The EMBO Journal (2012) 31, 417-428. doi:10.1038/emboj.2011.386; Published online 28 October 2011