Regulation of synaptic plasticity by microRNAs

神经细胞通过称为突触的特殊细胞间连接相互通信。突触的修饰是在发育和学习期间发生的可塑性的关键特征。脊椎动物可塑性的广泛研究的例子是长时程增强（LTP，一种持续的突触增强）和长时程抑制（LTD，一种持续的突触减弱）。虽然可塑性的短期事件是由蛋白质修饰介导的，但后期事件需要在突触处合成新蛋白质。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，这种情况如何发生的分子基础仍然难以捉摸。MicroRNA是最近发现的一类核酸，越来越多地被认为是蛋白质合成的关键调控因子。提示，神经元中的miRNA可以在突触附近检测到。为了进一步阐明在突触可塑性过程中miRNA在蛋白质合成中的作用，我们想分析在LTP或LTD后树突中的microRNA含量是否发生变化。识别在可塑性过程中受到调节的microRNA，并阐明突触蛋白质合成的控制机制，将大大提高我们对神经元发育以及学习和记忆的基本机制的认识。

Nerve cells communicate with each other via specialized intercellular junctions known as synapses. The modification of synapses is a key feature underlying plasticity that occurs during development and learning. Widely studied examples of vertebrate plasticity are long-term potentiation (LTP, a persistent synaptic enhancement) and long-term depression (LTD, a persistent synaptic weakening). While short-term events in plasticity are mediated by protein modifications, 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 basis of how this occurs remains elusive. MicroRNAs, a recently identified class of nucleic acids, are increasingly recognized as key regulators of protein synthesis. Suggestively, miRNAs in neurons can be detected close to synapses. To further elucidate the role of miRNAs in protein synthesis during synaptic plasticity we want to analyze whether the microRNA content in the dendrite changes after LTP or LTD. Identifying microRNAs that are regulated during plasticity and elucidating the control mechanisms for protein synthesis at the synapse will greatly enhance our knowledge of basic mechanisms underlying neuronal development as well as learning and memory.