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, June 2, 2014

Self-Tuning Neurons Promote Resilience to Stress, Depression

What is your doctor going to do based on this to handle your stress/depression on not being told of your objective diagnosis or any way to get to 100% recovery?
http://www.nih.gov/researchmatters/may2014/05052014resilience.htm
Enhancing brain mechanisms triggered by stress raised the resilience of mice to stress and relieved depression-like behaviors. The surprising results suggest novel approaches to promoting mental health.
Some mice exposed to repeated encounters with a dominant animal develop depression-like behaviors, while others don’t. Sensitive mice avoid other animals and lose their preference for sugar. In past work, a group of researchers led by Dr. Ming-Hu Han of the Icahn School of Medicine at Mount Sinai found that neurons in the ventral tegmental area (VTA)—one of the “reward” areas deep in the brain—fire at higher rates in mice that are more susceptible to social stress. These neurons are known to secrete the chemical messenger dopamine.
The scientists later found that mouse susceptibility to social stress could be turned on and off by manipulating the firing rates of these neurons. To explore how this mechanism works at the cellular level, the researchers focused on electrical events within the neurons. The study, funded in part by NIH’s National Institute of Mental Health (NIMH), appeared on April 18, 2014, in Science.
The researchers found that while stress-resilient mice had VTA dopamine neurons with stable firing rates and normal dopamine activity, these neurons had higher levels of an excitatory electrical current than those of stressed mice. The higher activation currents were accompanied by higher inhibitory potassium channel currents. The researchers hypothesized that, in resilient animals, runaway excitatory currents trigger a boost in inhibitory currents, resulting in normal mood-related behaviors.
The team thus tested whether boosting excitatory currents could activate compensatory currents in susceptible mice. Over 5 days, the scientists repeatedly infused the VTA of susceptible mice with a drug called lamotrigine, which is known to increase excitatory currents. The treated mice socialized more and their characteristic rodent sweet tooth came back. At the cellular level, these mice showed a marked increase in both excitatory and inhibitory currents, resulting in normal neuron activity. This self-tuning balance of activity, common in other body systems, is called homeostasis.
The scientists achieved similar results using a technique called optogenetics to activate neuronal activity. Further experiments showed that the homeostatic mechanism worked specifically in the reward circuit running from the VTA to cells in a brain area called the nucleus accumbens.
“To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” Han says. When an excitatory current develops in response to social stress—and is driven high enough for a sustained period—it triggers its own compensatory adaptation. Inhibitory currents correct out-of-balance electrical activity and thus produce resilience.
As counterintuitive as it seems, in this case, exaggerating an abnormality can be beneficial. Future strategies might harness this homeostatic mechanism to promote resilience to stress and combat depression.

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