Washington, Feb 20 (Inditop.com) Brain researcher Hiroshi Kawabe has uncovered the secret of nerve (brain) cell regeneration.
It is the working of a process that permits nerve cells to grow and form complex networks—something had been completely overlooked until now.
The study shows that an enzyme controls the structure of the cytoskeleton (cellular skeleton) and ensures that nerve cells can form the tree-like extensions that are necessary for signal transmission in the brain.
Nerve cells form complex extensions called dendrites (from Greek �dendron’ meaning tree), to be able to receive signals from billions of other cells.
The growth of dendrites takes place mainly during late embryonic and infantile brain development. During this phase, dendrites, stretching hundred of k1ilometres, end to end, grow from the 100 billion nerve cells in our brain.
The result is a highly-complex network of nerve cells that controls all bodily functions – from breathing to complicated learning processes.
In fact, a large number of signal processes control the direction and the speed of dendrite growth by influencing the structure of the cytoskeleton, which is inside the growing dendrite and responsible for its shape and extension.
G�ttingen-based brain researcher Hiroshi Kawabe has now discovered exactly how the growth of the cytoskeleton is controlled during the dendrite development.
Using specially bred genetically engineered mice, Kawabe, who conducts research at the Max Planck Institute for Experimental Medicine, discovered that the Nedd4-1 enzyme is essential for regular dendrite growth.
Nedd4-1 is an enzyme that usually controls the degradation of protein components in cells by combining them with another protein called ubiquitin.
The cell identifies these ubiquitinated molecules as “waste” and degrades them. In some cases, however, the ubiquitination does not lead to the degradation of the marked protein but changes its function instead.
Hiroshi Kawabe has now shown that the Nedd4-1 enzyme ubiquitinates a signal protein called Rap2, and thus prevents it causing the dismemberment of the cytoskeleton and the collapse of the dendrites.
“As long as Nedd4-1 is active, the nerve cell dendrites can grow normally,” said Kawabe.
“In its absence, the dendrite growth comes to a standstill and previously formed dendrites collapse, with dramatic consequences for the function of nerve cell networks in the brain.”
There are, however, probably a number of parallel operating signal paths which control the dendrite growth. This explains why nerve cells can also form dendrites without Nedd4-1 – albeit significantly fewer in number and shorter.
The Nedd4/Rap2/TNIK mechanism would then be only one of several that can partially compensate each other, said a Max Planck release.
These findings have been published in the February issue of Neuron.
