Center for Learning and Memory, Section of Neurobiology, Institute for Neuroscience, University of Texas, Austin, Texas 78712, USA.
Hippocampus. 2011 Apr;21(4):354-73. doi: 10.1002/hipo.20768.
Enlargement of dendritic spines and synapses correlates with enhanced synaptic strength during long-term potentiation (LTP), especially in immature hippocampal neurons. Less clear is the nature of this structural synaptic plasticity on mature hippocampal neurons, and nothing is known about the structural plasticity of inhibitory synapses during LTP. Here the timing and extent of structural synaptic plasticity and changes in local protein synthesis evidenced by polyribosomes were systematically evaluated at both excitatory and inhibitory synapses on CA1 dendrites from mature rats following induction of LTP with theta-burst stimulation (TBS). Recent work suggests dendritic segments can act as functional units of plasticity. To test whether structural synaptic plasticity is similarly coordinated, we reconstructed from serial section transmission electron microscopy all of the spines and synapses along representative dendritic segments receiving control stimulation or TBS-LTP. At 5 min after TBS, polyribosomes were elevated in large spines suggesting an initial burst of local protein synthesis, and by 2 h only those spines with further enlarged synapses contained polyribosomes. Rapid induction of synaptogenesis was evidenced by an elevation in asymmetric shaft synapses and stubby spines at 5 min and more nonsynaptic filopodia at 30 min. By 2 h, the smallest synaptic spines were markedly reduced in number. This synapse loss was perfectly counterbalanced by enlargement of the remaining excitatory synapses such that the summed synaptic surface area per length of dendritic segment was constant across time and conditions. Remarkably, the inhibitory synapses showed a parallel synaptic plasticity, also demonstrating a decrease in number perfectly counterbalanced by an increase in synaptic surface area. Thus, TBS-LTP triggered spinogenesis followed by loss of small excitatory and inhibitory synapses and a subsequent enlargement of the remaining synapses by 2 h. These data suggest that dendritic segments coordinate structural plasticity across multiple synapses and maintain a homeostatic balance of excitatory and inhibitory inputs through local protein-synthesis and selective capture or redistribution of dendritic resources.
树突棘和突触的增大与长时程增强 (LTP) 期间突触强度的增强相关,尤其是在不成熟的海马神经元中。不太清楚成熟海马神经元中这种结构突触可塑性的性质,也不知道 LTP 期间抑制性突触的结构可塑性。在这里,通过多核糖体系统地评估了在 theta 爆发刺激 (TBS) 诱导 LTP 后,来自成熟大鼠 CA1 树突上兴奋性和抑制性突触的结构突触可塑性和局部蛋白质合成的变化。最近的工作表明,树突段可以作为可塑性的功能单位。为了测试结构突触可塑性是否具有相似的协调性,我们从连续切片透射电子显微镜重建了在接受对照刺激或 TBS-LTP 的代表性树突段上接收刺激的所有棘突和突触。在 TBS 后 5 分钟,多核糖体在大棘突中升高,表明局部蛋白质合成的初始爆发,并且在 2 小时内,只有那些进一步扩大的突触的棘突包含多核糖体。在 5 分钟时,不对称轴突突触和短棘突的升高以及更多的非突触丝状伪足的升高证明了快速诱导的突触发生,在 30 分钟时更明显。在 2 小时时,最小的突触棘突数量明显减少。这种突触丢失被剩余兴奋性突触的增大完美地平衡,使得突触表面积的总和与树突段的长度成比例,并且在整个时间和条件下保持不变。值得注意的是,抑制性突触显示出平行的突触可塑性,也显示出数量的减少与突触表面积的增加完全平衡。因此,TBS-LTP 在 2 小时内引发棘突生成,随后小的兴奋性和抑制性突触丢失,剩余突触随后增大。这些数据表明,树突段通过局部蛋白质合成和树突资源的选择性捕获或重新分配,协调多个突触的结构可塑性,并维持兴奋性和抑制性输入的平衡。