Coordination of size and number of excitatory and inhibitory synapses results in a balanced structural plasticity along mature hippocampal CA1 dendrites during LTP.

Coordination of size and number of excitatory and inhibitory synapses results in a balanced structural plasticity along mature hippocampal CA1 dendrites during LTP.
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DOI:
10.1002/hipo.20768
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发表时间:
2011-04
期刊:
影响因子:
3.5
通讯作者:
Harris, Kristen M.
Harris, Kristen M.
中科院分区:
医学3区
文献类型:
--
作者:
Bourne, Jennifer N.;Harris, Kristen M.

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树突状刺和突触的扩大与长期增强期间突触强度增强相关,尤其是在未成熟的海马神经元中。这种结构突触可塑性在成熟的海马神经元上的性质尚不清楚,并且对LTP期间抑制性突触的结构可塑性一无所知。在这里,在用theta-burst刺激(TBS)诱导LTP后,在兴奋性和抑制性突触上,在兴奋性和抑制性突触上,在兴奋性和抑制性突触上,在兴奋性和抑制性突触上,在兴奋性和抑制性突触上对结构突触可塑性以及局部蛋白质合成的变化进行了时间和程度。最近的工作表明,树突状段可以充当可塑性的功能单位。为了测试结构突触可塑性是否类似地协调,我们从串行部分透射电子显微镜中重建了沿代表性的树突状段的所有刺和突触,都接受了控制刺激或TBS-LTP。 TBS后5分钟,在大棘中升高了多核糖体,表明最初的局部蛋白质合成爆发,并且只有2个小时,只有那些具有进一步增大突触的棘突含有多核糖体。在5分钟时,不对称轴突触和粗棘的升高和30分钟时更多的非突触丝霉素的升高证明了突触发生的快速诱导。到2小时,最小的突触棘的数量明显减少。通过扩大剩余的兴奋性突触的扩大,这种突触损失完全平衡,使得每长度的树突段的求和突触表面积在时间和条件上都是恒定的。值得注意的是,抑制性突触显示出平行的突触可塑性,这也表明数量下降完全由突触表面积的增加完全平衡。因此,TBS-LTP触发了旋转生成,然后引发了小兴奋性和抑制性突触的丧失,随后将其余突触扩大了2小时。这些数据表明,树突段协调了多个突触的结构可塑性,并通过局部蛋白质合成以及对树突状资源的选择性捕获或重新分布兴奋和抑制输入的体内平衡。
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 hr 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 hr, 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 hours. 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.
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