Resetting of ‘synaptic tags’ is time- and activity-dependent in rat hippocampal CA1in vitro
Resetting of ‘synaptic tags’ is time- and activity-dependent in rat hippocampal CA1in vitro
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体外大鼠海马 CA1 中“突触标签”的重置具有时间和活动依赖性
DOI：
10.1016/j.neuroscience.2004.08.014
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发表时间：
2004
期刊：
影响因子：
3.3
通讯作者：
Julietta Uta Frey
中科院分区：
文献类型：
--
作者：
Sreedharan Sajikumar;Julietta Uta Frey
我们最近提出，海马长期增强（LTP）和抑郁的维持取决于至少两个必要的过程：LTP的诱导必须设置(1)过程特异性“突触标签”，该标签捕获(2)过程非特异性可塑性相关蛋白（PRPs），通过异突触相互作用合成[Neurobiol Learn Mem 82(2004) 12]。“标签”和PRPs的特点是半衰期相对较短，几分钟到几个小时，然后很可能通过诸如去磷酸化之类的过程降解。现在的问题是，“标签”是否也可以以一种依赖于活动的方式重置，从而防止prp的加工产生短暂的短期可塑性。在这里，我们研究了早期LTP期间的这一主题，发现在早期LTP诱导后不久（5分钟）的低频刺激重置了大分子的“标签”或“标签复合物”，阻止了任何持久形式的LTP，从而阻止了记忆痕迹的形成。
We have recently proposed that the maintenance of hippocampal long-term potentiation (LTP) and depression depends on at least two required processes: induction of LTP must set (1) process-specific ‘synaptic tags’ which capture (2) process-unspecific plasticity-related proteins (PRPs), synthesized via a heterosynaptic interaction [Neurobiol Learn Mem 82 (2004) 12]. The ‘tag’ as well as the PRPs are characterized by a relatively short half-life of several minutes up to a few hours before they degrade most likely by processes such as dephosphorylation. The question now arose whether the ‘tags’ can also be reset in an activity-dependent manner, thus preventing the processing of PRPs with the result of transient short-lasting plasticity. Here we have investigated this topic during early-LTP and found that low-frequency stimulation shortly after early-LTP-induction (5 min) resets the ‘tag’ or the ‘tag complex’ of macromolecules preventing any lasting forms of LTP and thus, preventing the formation of a memory trace.