Deans' stroke musings: Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, October 31, 2011

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

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.