04 January 2024 | Manasi Iyer, Husniye Kantarci, Madeline H. Cooper, Nicholas Ambiel, Sammy Weiser Novak, Leonardo R. Andrade, Mable Lam, Graham Jones, Alexandra E. Münch, Xinzhu Yu, Baljit S. Khakh, Uri Manor & J. Bradley Zuchero
The study investigates the role of calcium signaling in oligodendrocyte myelination, focusing on the formation and morphology of myelin sheaths. Using genetic tools, the researchers attenuated calcium signaling in oligodendrocytes during development in a mouse model. Surprisingly, this attenuation did not affect the number of myelinated axons or myelin thickness but led to shorter and dysmorphic myelin sheaths. Mechanistically, calcium attenuation reduced actin filament levels in oligodendrocytes, and restoring actin filament levels partially rescued the myelin sheath defects. The findings suggest that calcium signaling regulates actin cytoskeletal assembly in nascent myelin sheaths, which is essential for accurate myelin morphology. This mechanism may allow myelin sheaths to respond to neuronal activity, fine-tuning conduction velocity and supporting learning and memory.The study investigates the role of calcium signaling in oligodendrocyte myelination, focusing on the formation and morphology of myelin sheaths. Using genetic tools, the researchers attenuated calcium signaling in oligodendrocytes during development in a mouse model. Surprisingly, this attenuation did not affect the number of myelinated axons or myelin thickness but led to shorter and dysmorphic myelin sheaths. Mechanistically, calcium attenuation reduced actin filament levels in oligodendrocytes, and restoring actin filament levels partially rescued the myelin sheath defects. The findings suggest that calcium signaling regulates actin cytoskeletal assembly in nascent myelin sheaths, which is essential for accurate myelin morphology. This mechanism may allow myelin sheaths to respond to neuronal activity, fine-tuning conduction velocity and supporting learning and memory.