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交流。突触可塑性，即突触的增强和减弱，是神经元发育的重要特征，也是学习和记忆形成的重要特征。被广泛研究的脊椎动物突触可塑性的例子是长期增强（持续的突触增强）和长期抑制（持续的突触减弱）。突触可塑性的短期事件是由蛋白质修饰介导的，而后期事件则需要突触合成新的蛋白质。某些信使rna被转运到突触并在突触上翻译，这一发现导致了长期可塑性是通过空间和暂时限制蛋白质合成来实现的概念。然而，导致诱导局部翻译的分子信号通路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.