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突触特异性的分子机制。

Molecular mechanisms of synaptic specificity.

机构信息

Howard Hughes Medical Institute and Department of Biology, Stanford University, Stanford, CA 94305-5020, USA.

出版信息

Mol Cell Neurosci. 2010 Mar;43(3):261-7. doi: 10.1016/j.mcn.2009.11.009. Epub 2009 Dec 5.

Abstract

Synapses are specialized junctions that mediate information flow between neurons and their targets. A striking feature of the nervous system is the specificity of its synaptic connections: an individual neuron will form synapses only with a small subset of available presynaptic and postsynaptic partners. Synaptic specificity has been classically thought to arise from homophilic or heterophilic interactions between adhesive molecules acting across the synaptic cleft. Over the past decade, many new mechanisms giving rise to synaptic specificity have been identified. Synapses can be specified by secreted molecules that promote or inhibit synaptogenesis, and their source can be a neighboring guidepost cell, not just presynaptic and postsynaptic neurons. Furthermore, lineage, fate, and timing of development can also play critical roles in shaping neural circuits. Future work utilizing large-scale screens will aim to elucidate the full scope of cellular mechanisms and molecular players that can give rise to synaptic specificity.

摘要

突触是神经元与其靶标之间传递信息的特化连接。神经系统的一个显著特征是其突触连接的特异性:单个神经元只会与一小部分可用的突触前和突触后伴侣形成突触。突触特异性传统上被认为是由跨突触间隙作用的黏附分子的同源或异源相互作用产生的。在过去的十年中,已经确定了许多产生突触特异性的新机制。突触可以由促进或抑制突触发生的分泌分子来特化,其来源可以是邻近的引导细胞,而不仅仅是突触前和突触后神经元。此外,谱系、命运和发育时间也可以在塑造神经回路中发挥关键作用。未来利用大规模筛选的工作将旨在阐明可以产生突触特异性的细胞机制和分子成分的全部范围。

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