The role of Ago1 and Ago2 in neuronal development and synaptic plasticty

神经细胞通过称为突触的特殊细胞间连接相互通信。突触可塑性是指突触的加强和减弱，是神经元发育以及学习和记忆形成的重要特征。脊椎动物突触可塑性的广泛研究的例子是长时程增强（持续的突触增强）和长时程抑制（持续的突触减弱）。突触可塑性中的短期事件由蛋白质修饰介导，而后期事件需要在突触处合成新的蛋白质。某些信使RNA被运输到突触并在突触处翻译的发现导致了长期可塑性是由空间和暂时限制的蛋白质合成实现的概念。然而，导致诱导局部翻译的分子信号传导途径在很大程度上仍然难以捉摸。

Nerve cells communicate with each other via specialized intercellular junctions known as synapses. Synaptic plasticity, which means the strengthening and weakening of synapses, is an important feature of neuronal development as well as for learning and memory formation. Widely studied examples of vertebrate synaptic plasticity are long-term potentiation (persistent synaptic enhancement) and long-term depression (persistent synaptic weakening). Short-term events in synaptic plasticity are mediated by protein modifications, while later events require the synthesis of new proteins at the synapse. The finding that certain messenger RNAs are transported to and translated at the synapse led to the notion that long-term plasticity is implemented by spatially and temporarily restricted protein synthesis. However, the molecular signaling pathways leading to the induction of local translation remain largely elusive.