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

A couple of interesting concepts here, NO, nitric oxide needed for synaptic plasticity, useful for neuroplasticity(I think). A suggestion NO is involved in NO-induced neuronal cell death. Hey, more research needed. Should NO be a hyperacute therapy or not?
http://www.nature.com/emboj/journal/vaop/ncurrent/full/emboj2011386a.html

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

Abstract

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.