Deans' stroke musings: A Key Role for TRPM7 Channels in Anoxic Neuronal Death

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.

Saturday, November 30, 2013

A Key Role for TRPM7 Channels in Anoxic Neuronal Death

Maybe #1 in my list of neuronal cascade of death items is not really a problem. Or at least not an easy problem to solve.
1. Excitotoxicity
2. Glutamate poisoning
3. Capillaries that don't open due to pericytes
4. Inflammatory action leaking through the blood brain barrier
5. Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death.
6. Reperfusion injury
http://www.cell.com/retrieve/pii/S0092867403010171

Cell, Volume 115, Issue 7, 863-877, 26 December 2003
Copyright © 2003 Cell Press All rights reserved.

Authors

Michelle Aarts, Koji Iihara, Wen-Li Wei, Zhi-Gang Xiong, Mark Arundine, Waldy Cerwinski, John F. MacDonald, Michael Tymianski send email

See Affiliations

Abstract

Excitotoxicity in brain ischemia triggers neuronal death and neurological disability, and yet these are not prevented by antiexcitotoxic therapy (AET) in humans. Here, we show that in neurons subjected to prolonged oxygen glucose deprivation (OGD), AET unmasks a dominant death mechanism perpetuated by a Ca²⁺-permeable nonselective cation conductance (I_OGD). I_OGD was activated by reactive oxygen/nitrogen species (ROS), and permitted neuronal Ca²⁺ overload and further ROS production despite AET. I_OGD currents corresponded to those evoked in HEK-293 cells expressing the nonselective cation conductance TRPM7. In cortical neurons, blocking I_OGD or suppressing TRPM7 expression blocked TRPM7 currents, anoxic ⁴⁵Ca²⁺ uptake, ROS production, and anoxic death. TRPM7 suppression eliminated the need for AET to rescue anoxic neurons and permitted the survival of neurons previously destined to die from prolonged anoxia. Thus, excitotoxicity is a subset of a greater overall anoxic cell death mechanism, in which TRPM7 channels play a key role.