Axons play a vital role in the nervous system in transmitting signals from one nerve cell to the dendrites on the other. Researchers from the Howard Hughes Medical Institute and the University of Wisconsin tested with the removal of protein to study brain development and found that the removal of one key protein from neurons obstructs the transportation of other vital proteins thus stunts the growth and development of axons.
In a study led by Edwin Chapman of the Howard Hughes Medical Institute and a team from the University of Wisconsin–Madison reported that the growth of axons is stopped due to the cease in the production of synaptotagmin 17 (syt-17) protein. Accelerated axon growth occurs with the excessive production of syt-17 which is also problematic, as it leads to neurodegenerative disorders or spinal cord diseases.
These findings from the study are published in the Nature Communications journal.
It was discovered that the 17th(and last) synaptotagmin gene is responsible for the synaptotagmin protein production in the human body. Edwin Chapman says; “Lots of work has been done on this family since it was discovered in 1981.”
Synaptotagmin proteins are also responsible for the release of neurotransmitters, chemical messengers transported through nerve cells to aid the process of communication. Synaptotagmin proteins serve as calcium sensors thus carry out this process in the presence of calcium ions.
Chapman says; “Calcium ions are a basic signal in the nervous system, and so synaptotagmin proteins have been intensely studied.”
In an attempt to search the exact location of synaptotagmin proteins in the neurons, Chapman and first author of the research David Ruhl traced syt-17 to the Golgi apparatus. Golgi apparatus, a shipping center inside the neuron that plays a role in the “Packaging” of the proteins for delivery from another part of the cell to the end of an axon.
“It’s a bit of a simplification, basically, you can’t build without supplies, and one of the ways that neurons are able to build such long, complicated axons is through syt-17 speeding up the production line.”, Chapman said.
About six years ago, while searching different synaptotagmin proteins inside the neurons, Chapman discovered that syt-17 aids in the growth of axon. “We made an accidental discovery that it makes axons grow really long,” Chapman says. “Well, that was interesting! We decided to work on it.”
In mice model with eliminated syt-17 gene, reported axons hardly grow in the absence of this gene while the presence of the gene aided with the growth of the axons. Chapman says. “But in mice genetically programmed to make an abnormally large quantity of syt-17, the axons grew much faster than normal.”
Chapman says. “To grow an axon, you’ve got to send a lot of stuff down pipelines that supply the growing end of an axon. Think of building a house: You need shipments of studs, floor joists, and roof shingles. A growing axon needs its own parcels, though they are much smaller.”
The postdoctoral researcher at the University of California Mr. Ruhl reported that the syt-17 protein unexpectedly has two stashes; first stash on the signal-shipping side in the axon, the second in the signal-sensing side in the dendrite, on the synapse. Syt-17 protein had two completely unrelated properties.
“It’s the exact opposite of what we’d have guessed,” says Ruhl. “I think the second function is pretty cool.”
The syt-17 stash at the dendrite serves as a reserve of receptors inside the cells, the neurotransmitters in the synapse binds with these receptors thus aids in synaptic communication. Synapse is the junction between two nerve cells.
“Without syt-17 (at the dendrite) most of the receptors wind up on the surface and synapses are turned up to 11,” he says. This helps in forming the ability of individuals to adapt and learn. “In plasticity, an important feature is increasing or decreasing receptivity to neurotransmitters,” Chapman says. Without this phenomenon, neurons may result in uncontrollable firing of signals, thus leading to problems like seizures.
Chapman says; so syt-17 has “a key player in the negative half of the balance sheet,”. “It doesn’t just help axons grow; it regulates how existing synapses respond to signals.”
Like a hard disk drive in computers, the brain needs to recycle old information in order to make “room” for storing new information. “Remembering is important, but forgetting is important, too.”