Dendritic spine dynamics are regulated by monocular deprivation and extracellular matrix degradation
Dendritic spine dynamics are regulated by monocular deprivation and extracellular matrix degradation
复制标题
DOI：
10.1016/j.neuron.2004.12.001
复制
发表时间：
2004-12-16
期刊：
影响因子：
16.2
通讯作者：
Sur, M
中科院分区：
文献类型：
--
作者：
Oray, S;Majewska, A;Sur, M
哺乳动物初级视觉皮层（V1）在一个明确界定的关键期内对视觉输入的变化尤为敏感，在此期间，闭上一只眼睛会导致神经元对被剥夺视觉的眼睛的反应性丧失，并使反应向睁开的眼睛转移。这种功能可塑性可能迅速发生，即使仅闭眼一天也会如此，尽管这些变化的结构基础尚不清楚。在此，我们表明，在短暂的单眼剥夺后，树突棘水平会发生快速的结构变化。这些变化在双眼区的颗粒上层和颗粒下层明显可见，并且可以通过组织型纤溶酶原激活剂/纤溶酶蛋白水解级联反应引起的细胞外基质降解来模拟。此外，单眼剥夺会阻断基质降解随后产生的效应，这表明该机制在体内是活跃的，以允许在眼优势可塑性期间进行结构重塑。
The mammalian primary visual cortex (V1) is especially susceptible to changes in visual input over a well-defined critical period, during which closing one eye leads to a loss of responsiveness of neurons to the deprived eye and a shift in response toward the open eye. This functional plasticity can occur rapidly, following even a single day of eye closure, although the structural bases of these changes are unknown. Here, we show that rapid structural changes at the level of dendritic spines occur following brief monocular deprivation. These changes are evident in the supra- and infragranular layers of the binocular zone and can be mimicked by degradation of the extracellular matrix with the tPA/plasmin proteolytic cascade. Further, monocular deprivation occludes a subsequent effect of matrix degradation, suggesting that this mechanism is active in vivo to permit structural remodeling during ocular dominance plasticity.