Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

作者：Kakizawa Sho^*; Yamazawa Toshiko; Chen Yili; Ito Akihiro; Murayama Takashi; Oyamada Hideto; Kurebayashi Nagomi; Sato Osamu; Watanabe Masahiko; Mori Nozomu; Oguchi Katsuji; Sakurai Takashi; Takeshima Hiroshi; Saito Nobuhito; Iino Masamitsu

来源：The EMBO Journal, 2012, 31(2): 417-428.

DOI：10.1038/emboj.2011.386

• calcium
• nitric oxide
• ryanodine receptor
• synapse

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

• 出版日期2012-1-18