【原】eIF4F formation, Synaptic Plasticity, and Memory

The Translation Repressor 4E-BP2 Is Critical for eIF4F Complex Formation, Synaptic Plasticity, and Memory in the Hippocampus

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|核心内容：

长时间的突触可塑性和记忆需要mRNA翻译，但目前尚不清楚如何调节这一过程。

为了探讨翻译抑制剂4E-BP2在海马长时程增强(LTP)和学习记忆中的作用，我们对4E-BP2敲除小鼠进行了研究。 

有趣的是，在Schaffer侧支通路中，4E-BP2的敲除将早期LTP转化为晚期LTP(L-LTP)，这可能是由于eIF4F复合物的形成和翻译起始增加所致。 

在4E-BP2敲除小鼠中，由于传统刺激范式诱导的L-LTP受到阻碍，这揭示了4E-BP2是活性诱导翻译的一个重要抑制子。 

此外，4E-BP2敲除小鼠还表现出空间学习和记忆受损和条件恐惧联想记忆缺陷。 

这些结果表明，在LTP和小鼠海马学习记忆过程中，4E-BP2对eIF4F复合物的适当调节起着至关重要的作用。

原文摘要：

 Long-lasting synaptic plasticity and memory requires mRNAtranslation, yet little is known asto howthis process is regulated. To explore the role that the translation repressor 4E-BP2 plays in hippocampal long-term potentiation (LTP) and learning and memory, we examined 4E-BP2 knock-out mice. Interestingly, genetic elimination of 4E-BP2 converted early-phase LTP to late-phase LTP (L-LTP) in the Schaffer collateral pathway, likely as a result of increased eIF4F complex formation and translation initiation. A critical limit for activityinduced translation was revealed in the 4E-BP2 knock-out mice because L-LTP elicited by traditional stimulation paradigms was obstructed. Moreover, the 4E-BP2 knock-out mice also exhibited impaired spatial learning and memory and conditioned fear-associative memory deficits. These results suggest a crucial role for proper regulation of the eIF4F complex by 4E-BP2 during LTP and learning and memory in the mouse hippocampus.