News Discovery of Calcium Channel Crucial to Myelin Formation May Provide New MS-treatment Leads Discovery of Calcium Channel Crucial to Myelin Formation May Provide New MS-treatment Leads by Patricia Silva, PhD | December 12, 2016 Share this article: Share article via email Copy article link A specific type of channel that facilitates calcium flow is needed for normal development of cells that produce a shield, called myelin, around nerve fibers ā a finding that could open up new approaches to regenerating the myelin-producing cells (called oligodendrocytes) lost in multiple sclerosis (MS). Researchers now hope to find ways to manipulate calcium channels after an injury that leads to oligodendrocyte-cell dysfunction and to regenerate these cells.Ā Since plenty of drugs targeting calcium channels already exist for other diseases, the team hopes that knowledge from other fields will help advance their research. The study,Ā āConditional Deletion of the L-Type Calcium Channel Cav1.2 in Oligodendrocyte Progenitor Cells Affects Postnatal Myelination in Mice,āĀ was published in theĀ Journal of Neuroscience. AĀ University at BuffaloĀ (UB) research team using mice to study myelin damage and regeneration discovered that, when a particular calcium channel worked normally, oligodendrocyte cells matured and myelin was formed. āOur findings show that these calcium channels modulate the maturation of oligodendrocytes in the brain after birth,ā Pablo M. Paez, PhD, the leader author of the study, said in aĀ news release. āThatās important because itās possible that the activity of this calcium channel can be manipulated pharmacologically to encourage oligodendrocyte maturation and remyelination after demyelinating episodes in the brain.” Paez is an assistant professor in the Department of Pharmacology and Toxicology at theĀ Jacobs School of Medicine and Biomedical SciencesĀ at UB and a research scientist at the university’sĀ Hunter James Kelly Research InstituteĀ (HJKRI). When the team removed the voltage-controlled calcium channel in cells destined to become oligodendrocytes, the mice did not develop normal amounts of myelin. In addition, the cells themselves did not mature into oligodendrocytes. And the abnormalities persisted until the animals became adults. āIf we can further enhance our understanding of how these oligodendrocyte precursor cells mature, then it may be possible to stimulate them to replace myelin in diseases like multiple sclerosis,ā Paez said. Paez said therapies targeting calcium channels are often used to manage heart disease and other disorders. āThe pharmacology of these calcium channel blockers is very well-understood, so an understanding of how they influence myelination could potentially bring us closer to new therapies more rapidly than some other therapeutic possibilities,ā said Lawrence Wrabetz, MD, professor of neurology and biochemistry and director at the HJKRI, who was not involved in the research. Print This Page About the Author Patricia Silva, PhD PatrĆcia holds a PhD in medical microbiology and infectious diseases from the Leiden University Medical Center, Netherlands, and completed a postdoctoral research fellowship at the Instituto de Medicina Molecular, Lisbon, Portugal. Her work in academia was mainly focused on molecular biology and the genetic traits of infectious agents such as viruses and parasites. PatrĆcia earned several travel awards to present her work at international scientific meetings. She is a published author of several peer-reviewed science articles. Tags myelin, oligodendrocyte
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