Associate Professor of Biology and Neuroscience Hebe Guardiola-Diaz recently teamed up with researchers at the University of Connecticut to study the development and stability of oligodendrocytes, cells in the brain that produce the myelin required for nervous system function.
During a 2009-2010 sabbatical, Guardiola-Diaz spent time as a visiting faculty member at the UConn Health Center, working with Rashmi Bansal, a professor of neuroscience at UConn. Guardiola-Diaz spent this time focused on a process known as oligodendrocyte differentiation. Guardiola-Diaz explained, “Oligodendrocyte are cells in the brain that make myelin, which is a fatty substance that protects nerve cells and makes it possible for them to communicate efficiently with their targets.”
The deterioration of myelin around neurons can lead to a number of degenerative nerve diseases, the most common example of which is multiple sclerosis. “Because of this, it is important to understand how oligodendtocytes develop and the properties that allow them to survive in dynamic interaction with their axons,” Guardiola-Diaz said.
One result of this research partnership was an article that was co-authored by Guardiola-Diaz, Bansal, and Akihiro Ishii, a postdoctoral fellow at UConn and advisee of Bansal. The article specifically examines a signaling network of proteins inside neurons that convey information from the cell’s environment. “The paper describes selective use of the signaling proteins Erk1/2MAPK and mTOR during different stages of oligodendrocyte development,” says Guardiola-Diaz. “We’re asking questions like, ‘What is it that mTOR does inside cells that is so essential? Why does interfering with this protein disrupt the developmental process of oligodendrocytes?’”
Guardiola-Diaz and her co-authors carried out their research on isolated cells in culture under controlled conditions. She points out that colleagues in the field of neuroscience are currently carrying out similar research in vivo—or within a living organism—by using new technologies that enable scientists to disrupt genes in animal models for human disorders. “As we find out more about the signaling requirements at different stages of oligodendrocyte development, we will better understand their functional interaction with neurons in the healthy and diseased brain.”
Click here to read the abstract.