Pratt Kara G, Watt Alanna J, Griffith Leslie C, Nelson Sacha B, Turrigiano Gina G
Department of Biology, Volen National Center for Complex Systems, Brandeis University, Waltham, MA 02454, USA.
Neuron. 2003 Jul 17;39(2):269-81. doi: 10.1016/s0896-6273(03)00422-7.
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.
竞争性突触重塑是发育可塑性的一个重要特征，但其分子机制在很大程度上仍不清楚。钙/钙调蛋白依赖性蛋白激酶II（CaMKII）可诱导突触强度的突触后变化。我们发现，突触后CaMKII也会在培养的皮质神经元之间产生结构性突触重排。激活的CaMKII（T286D）的突触后表达使成对锥体神经元之间的传递强度增加了4倍，这是通过量子幅度的适度增加和突触接触数量的更大增加实现的。同时，T286D降低了总体兴奋性突触密度，并增加了未连接对的比例。这表明一些突触伙伴之间的连接性增加，而其他伙伴则被消除。连接性的增强需要活性和NMDA受体激活，而消除则不需要。这些数据表明，CaMKII的突触后激活会诱导突触前输入的结构重塑，有利于保留活跃的突触前伙伴。
