So our stroke associations should be sponsoring research to find out how to recover proprioception now that we have found this protein. Yes this is a BHAG(Big Hairy Audacious Goal). I don't care, leaders solve the difficult problems, they don't run away from them. If you are running away, then resign and let someone with more initiative take your place.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=158221&CultureCode=en
Can you touch a finger to the tip of your nose with your eyes closed?
Most of us can, thanks to a sense called proprioception, which tells us
where our body parts are relative to each other and our environment.
Not surprisingly, this sense is essential for normal movement and
balance—walking, for instance.
For decades, biologists have been trying to find the crucial sensor
protein in nerve endings that translates muscle and tendon stretching
into proprioceptive nerve signals. Now in a study published in Nature Neuroscience
on November 9, 2015, a team led by scientists from The Scripps Research
Institute (TSRI) has identified this sensor protein in mice.
It turns out to be a protein called Piezo2, which was found recently to mediate the sense of touch.
“To the layman it might not seem surprising that touch and
proprioception would use the same sensor protein, but within this field
there has been a lot of evidence suggesting otherwise—so finding that
Piezo2 does both was a surprise,” said lead investigator Ardem
Patapoutian, a professor at TSRI and investigator with Howard Hughes
Medical Institute.
The laboratories of Thomas M. Jessell at Columbia University and
Katherine A. Wilkinson at San Jose State University collaborated on the
study.
Multi-Purpose Protein
Patapoutian and his laboratory specialize in identifying and
characterizing sensory transducer proteins and over the past 15 years
have identified transducers of cold, heat and pain. In two studies
published last year, they identified Piezo2 as the principal sensor for
ordinary, non-painful touch in mice.
The new findings stem in part from those studies, in which
Patapoutian and his team developed transgenic mice that can be made to
switch off Piezo2 activity in “touch” neurons and other sensory neurons
based in the spine. With Piezo2 silenced, the mice showed profound
deficits in responding to touch. But they also showed a different kind
of deficit.
“Their walking was a bit abnormal, which gave us a hint that some
proprioceptive neurons might be affected, too,” said Seung-Hyun Woo, a
research associate in the Patapoutian laboratory who was first author of
the new study.
In an initial set of experiments for the new study, the team managed
to isolate mouse sensory neurons involved in proprioception and tested
these neurons’ electrical responses to mild mechanical pressure. Such
neurons’ nerve ends and cell bodies are known to be studded with
mechanically activated ion channel proteins, which essentially spring
open—admitting a surge of charged molecules (ions) and triggering an
electrical nerve impulse—when the surrounding nerve or cell membrane is
distorted sufficiently by a stretching of the local muscle tissue. Prior
studies had suggested that the main stretch-sensing protein expressed
by proprioceptive neurons is one that specializes in admitting sodium
ions. However, the team found evidence from these initial tests that the
main ion-channel protein on proprioceptive neurons is not a selective
sodium-channel protein, but in fact has properties consistent with
Piezo2s.
The researchers then confirmed that Piezo2 is expressed in mouse
proprioceptive neurons and their muscle-embedded nerve ends. To
establish Piezo2’s role with more certainty, they developed two lines of
transgenic mice in which Piezo2 production could be switched off in
proprioceptive neurons shortly after the mice were born. The resulting
animals showed severe abnormalities in walking and limb positioning.
“Their limbs were everywhere — they looked like they were trying to do yoga,” said Woo.
In a final set of experiments, the team found that leg muscle tissue
from these mice lacking Piezo2—tissue with proprioceptive nerves
embedded—produced almost no nerve signals in response to muscle
stretching, whereas muscle tissue from normal mice produced robust
signals.
“The data that we have now in support of Piezo2’s role in proprioception are really overwhelming,” said Patapoutian.
While the finding is a milestone in sensory neuroscience, it may also
lead to a better understanding of some human diseases relating to
proprioception. For example, a genetic disorder known as distal
arthrogryposis type 5, whose sufferers are born with severely contracted
joints, was found in 2013—by Patapoutian and colleagues—to be caused by
a mutation to the human version of Piezo2.
The Patapoutian lab is continuing to investigate.
The other co-authors of the paper, “Piezo2 is the principal
mechanotransduction channel for proprioception,” were Viktor Lukacs and
Allain Francisco from TSRI, Joriene C de Nooij from Columbia University,
and Dasha Zaytseva and Connor R. Criddle from San Jose State
University.
Funding was provided by the Howard Hughes Medical Institute and the National Institutes of Health (R01DE022358).
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 28,987 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
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.
Subscribe to:
Post Comments (Atom)
No comments:
Post a Comment