The ubiquitin proteasome system functions as an inhibitory constraint on synaptic strengthening.
The ubiquitin proteasome system functions as an inhibitory constraint on synaptic strengthening.
复制标题
泛素蛋白酶体系统对突触强化起到抑制性约束作用。
DOI：
10.1016/s0960-9822(03)00332-4
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Martin,KelseyC
中科院分区：
文献类型：
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作者：
Zhao,Yali;Hegde,AshokN;Martin,KelseyC
背景：突触可塑性的持久形式已被证明依赖于基因表达的变化。虽然许多研究都集中在学习相关的突触可塑性的转录和翻译的调节，调节蛋白质降解提供了另一种常见的手段，改变大分子组成的cells.Results：我们已经调查了泛素蛋白酶体系统中的作用，在长期持久的形式学习相关的可塑性inAsymasensory-motor突触。我们发现，抑制蛋白酶体产生一个持久的（24小时）增加感觉和运动神经元之间的突触强度，它显着提高了马槟榔诱导的长期便利。由蛋白酶体抑制剂产生的突触强度的增加依赖于翻译而不是转录。除了增加突触强度外，蛋白酶体抑制还导致感觉神经元和运动神经元之间形成的突触接触数量增加。阻断分离的突触后运动神经元中的蛋白酶体产生的谷氨酸诱发的突触后电位的增加，和阻断分离的突触前感觉细胞中的蛋白酶体产生的神经突长度和branching.Conclusions增加：我们得出结论，前和突触后底物的泛素蛋白酶体的功能组成性地调节突触强度和生长，泛素蛋白酶体通路的功能在成熟的神经元作为抑制约束突触强化。
Background:Long-lasting forms of synaptic plasticity have been shown to depend on changes in gene expression. Although many studies have focused on the regulation of transcription and translation during learning-related synaptic plasticity, regulated protein degradation provides another common means of altering the macromolecular composition of cells.Results:We have investigated the role of the ubiquitin proteasome system in long-lasting forms of learning-related plasticity inAplysiasensory-motor synapses. We find that inhibition of the proteasome produces a long-lasting (24 hr) increase in synaptic strength between sensory and motor neurons and that it dramatically enhances serotonin-induced long-term facilitation. The increase in synaptic strength produced by proteasome inhibitors is dependent on translation but not transcription. In addition to the increase in synaptic strength, proteasome inhibition leads to an increase in the number of synaptic contacts formed between the sensory and motor neurons. Blockade of the proteasome in isolated postsynaptic motor neurons produces an increase in the glutamate-evoked postsynaptic potential, and blockade of the proteasome in the isolated presynaptic sensory cells produces increases in neurite length and branching.Conclusions:We conclude that both pre- and postsynaptic substrates of the ubiquitin proteasome function constitutively to regulate synaptic strength and growth and that the ubiquitin proteasome pathway functions in mature neurons as an inhibitory constraint on synaptic strengthening.