Activity-induced targeting of profilin and stabilization of dendritic spine morphology
Activity-induced targeting of profilin and stabilization of dendritic spine morphology
复制标题
DOI：
10.1038/nn1135
复制
发表时间：
2003-11-01
影响因子：
25
通讯作者：
Matus, A
中科院分区：
文献类型：
--
作者：
Ackermann, M;Matus, A
树突棘的形态变化与脑回路中的连接可塑性有关，但从突触传递到结构变化的潜在途径尚不清楚。使用表达GFP标记的蛋白质的原代神经元，我们发现，profilin，肌动蛋白聚合的调节剂，有针对性的脊柱头部时，突触后NMDA受体被激活，并在脊柱形状的肌动蛋白为基础的变化被伴随封锁。Profilin靶向是由电刺激模式触发的，已知电刺激模式可诱导与记忆形成相关的突触反应性的长期变化。这些结果表明，除了电生理变化，NMDA受体激活启动树突棘的肌动蛋白细胞骨架的变化，稳定突触结构。
Morphological changes in dendritic spines have been implicated in connective plasticity in brain circuitry, but the underlying pathway leading from synaptic transmission to structural change is unknown. Using primary neurons expressing GFP-tagged proteins, we found that profilin, a regulator of actin polymerization, is targeted to spine heads when postsynaptic NMDA receptors are activated and that actin-based changes in spine shape are concomitantly blocked. Profilin targeting was triggered by electrical stimulation patterns known to induce the long-term changes in synaptic responsiveness associated with memory formation. These results suggest that, in addition to electrophysiological changes, NMDA receptor activation initiates changes in the actin cytoskeleton of dendritic spines that stabilize synaptic structure.