Activity-dependent remodeling of presynaptic inputs by postsynaptic expression of activated CaMKII
Activity-dependent remodeling of presynaptic inputs by postsynaptic expression of activated CaMKII
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DOI：
10.1016/s0896-6273(03)00422-7
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发表时间：
2003-07-17
期刊：
影响因子：
16.2
通讯作者：
Turrigiano, GG
中科院分区：
文献类型：
--
作者：
Pratt, KG;Watt, AJ;Turrigiano, GG
竞争性突触重塑是发育可塑性的重要特征，但其分子机制尚不清楚。钙/钙调蛋白依赖的蛋白激酶II(CaMKII)可引起突触后突触强度的改变。我们发现，突触后CaMKII也在培养的皮质神经元之间产生结构性突触重排。突触后表达激活的CaMKII(T286D)使锥体神经元对之间的传递强度增加4倍，这是通过适度增加量子幅度和较大增加突触接触数量来实现的。同时，T286D降低了整体兴奋性突触密度，增加了未连接对的比例。这表明，来自一些突触伙伴的连接性增加了，而其他伙伴则被排除了。连接性的增强需要活性和NMDA受体的激活，而消除则不需要。这些数据表明，突触后激活CaMKII诱导了突触前输入的结构性重构，这有利于活跃的突触前伙伴的保留。
Competitive synaptic remodeling is an important feature of developmental plasticity, but the molecular mechanisms remain largely unknown. Calcium/calmodulin-dependent protein kinase II (CaMKII) can induce postsynaptic changes in synaptic strength. We show that postsynaptic CaMKII also generates structural synaptic rearrangements between cultured cortical neurons. Postsynaptic expression of activated CaMKII (T286D) increased the strength of transmission between pairs of pyramidal neuron by a factor of 4, through a modest increase in quantal amplitude and a larger increase in the number of synaptic contacts. Concurrently, T286D reduced overall excitatory synaptic density and increased the proportion of unconnected pairs. This suggests that connectivity from some synaptic partners was increased while other partners were eliminated. The enhancement of connectivity required activity and NMDA receptor activation, while the elimination did not. These data suggest that postsynaptic activation of CaMKII induces a structural remodeling of presynaptic inputs that favors the retention of active presynaptic partners.