核心概念
Oligodendrocyte maturation and myelination during adolescence act as a functional brake on neuronal plasticity in the visual cortex.
摘要
The article investigates the relationship between oligodendrocyte maturation, myelination, and neuronal plasticity in the visual cortex. It presents evidence that the developmental process of myelination by oligodendrocytes plays a critical role in shaping the maturation and stabilization of cortical circuits, thereby limiting neuronal plasticity as animals age.
The key findings are:
- During adolescence, visual experience modulates the rate of oligodendrocyte maturation in the visual cortex.
- Genetically blocking oligodendrocyte differentiation and myelination in adolescent mice leads to enhanced functional plasticity in the adult visual cortex, as evidenced by a significant decrease in responses to the deprived eye following a brief period of monocular deprivation.
- This enhanced plasticity is accompanied by greater turnover of dendritic spines and coordinated reductions in spine size following deprivation.
- Inhibitory synaptic transmission, which gates experience-dependent plasticity at the circuit level, is diminished in the absence of adolescent oligodendrogenesis.
These results support the concept that developmental myelination by oligodendrocytes acts as a functional brake on neuronal plasticity, stabilizing cortical circuits as animals mature.
统计
Developmental myelination is a protracted process in the mammalian brain.
Visual experience modulated the rate of oligodendrocyte maturation in the visual cortex during adolescence.
In adult mice lacking adolescent oligodendrogenesis, a brief period of monocular deprivation led to a significant decrease in visual cortex responses to the deprived eye.
引用
"One theory for why oligodendrocytes mature so slowly posits that myelination may stabilize neuronal circuits and temper neuronal plasticity as animals age."
"These results establish a critical role for oligodendrocytes in shaping the maturation and stabilization of cortical circuits and support the concept of developmental myelination acting as a functional brake on neuronal plasticity."