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.

Sunday, December 4, 2011

neuron pathfinding and fillipodia

I found both of these from reading a neuro blogger. I think we need more research on how to express them in our brains. If we expect neurogenesis or neuroplasticity to reach intact brain then this process needs to be developed so we can point the neurons in the correct direction. For example, supposedly my sensory cortex was not damaged in my stroke but my sensation is less than before on my left side. Based on this and the fact my MCA plugged I have to make an assumption that the white matter underlying the sensory cortex is dead and thus I need to reroute new neuron spikes to the sensory cortex. This should have come from my doctor but I had to do all this investigation myself.
from Wikipedia;
Developing neuron axons have growth cones at the ends of their growing tips. Growth cones have many long, thin, finger-like projections called fillipodia.
A growth cone is a dynamic, actin-supported extension of a developing axon seeking its synaptic target. Their existence was originally proposed by Spanish histologist Santiago Ramón y Cajal based upon stationary images he observed under the microscope. He first described the growth cone based on fixed cells as “a concentration of protoplasm of conical form, endowed with amoeboid movements” (Cajal, 1890).[1] Neuronal growth cones are situated on the very tips of nerve cells on structures called axons and dendrites. The sensory, motor, integrative, and adaptive functions of growing axons and dendrites are all contained within this specialized structure.

Structure


Two fluorescently-labeled growth cones. The growth cone (green) on the left is an example of a “filopodial” growth cone, while the one on the right is a “lamellipodial” growth cone. Typically, growth cones have both structures, but with varying sizes and numbers of each.
The morphology of the growth cone can be easily described by using the hand as an analogy. The fine extensions of the growth cone are known as "filopodia" or microspikes. The filopodia are like the "fingers" of the growth cone; they contain bundles of actin filaments (F-actin) that give them shape and support. Filopodia are the dominant structures in growth cones, and they appear as narrow cylindrical extensions which can extend several micrometres beyond the edge of the growth cone. The filopodia are bound by membrane which contains receptors and cell adhesion molecules that are important for axon growth and guidance.
In between filopodia--much like the webbing of the hands--are the "lamellipodia". These are flat regions of dense actin meshwork instead of bundled F-actin as in filopodia. They often appear adjacent to the leading edge of the growth cone and are positioned between two filopodia, giving them a “veil-like” appearance. In growth cones, new filopodia usually emerge from these inter-filopodial veils.
The growth cone is described in terms of three regions: the peripheral (P) domain, the transitional (T) domain, and the central (C) domain. The peripheral domain is the thin region surrounding the outer edge of the growth cone. It is composed primarily of an actin-based cytoskeleton, and contains the lamellipodia and filopodia which are highly dynamic. Microtubules, however, are known to transiently enter the peripheral region via a process called dynamic instability. The central domain is located in the center of the growth cone nearest to the axon. This region is composed primarily of a microtubule-based cytoskeleton, is generally thicker, and contains many organelles and vesicles of various sizes. The transitional domain is the region located in the thin band between the central and peripheral domains.
There are also many cytoskeletal-associated proteins, which perform a variety of duties within the growth cone, such as anchoring actin and microtubules to each other, to the membrane, and to other cytoskeletal components. Some of these components include molecular motors that generate force within the growth cone and membrane-bound vesicles which are transported in and out of the growth cone via microtubules. Some examples of cytoskeletal-associated proteins are Fascin and Filamin (actin bundling), Talin (actin anchoring), myosin (vesicle transport), and mDia (microtubule-actin linking).

Axon branching and outgrowth

The highly dynamic nature of growth cones allows them to respond to the surrounding environment by rapidly changing direction and branching in response to various stimuli

No comments:

Post a Comment