Olsen Olav, Moore Kimberly A, Nicoll Roger A, Bredt David S
Departments of Physiology and Cellular & Molecular Pharmacology, University of California-San Francisco, 600 16th Street, San Francisco, CA, USA.
Curr Opin Cell Biol. 2006 Apr;18(2):223-7. doi: 10.1016/j.ceb.2006.02.010. Epub 2006 Feb 28.
Neurotransmission requires proper organization of synaptic vesicle pools and rapid release of vesicle contents upon presynaptic depolarization. Genetic studies have begun to reveal a critical role for scaffolding proteins in such processes. Mutations in genes encoding components of the highly conserved MALS/CASK/Mint-1 complex cause presynaptic defects. In all three mutants, neurotransmitter release is reduced in a manner consistent with aberrant vesicle cycling to the readily releasable pool. Recently, liprin-alpha proteins, which define active zone size and morphology, were found to associate with MALS/CASK, suggesting that this complex links the presynaptic release machinery to the active zone, thereby regulating neurotransmitter release.
神经传递需要突触小泡池的适当组织以及在突触前去极化时小泡内容物的快速释放。遗传学研究已开始揭示支架蛋白在这些过程中的关键作用。编码高度保守的MALS/CASK/Mint-1复合体组分的基因突变会导致突触前缺陷。在所有这三种突变体中，神经递质释放均以与异常小泡循环至易释放池相一致的方式减少。最近，发现可定义活性区大小和形态的liprin-α蛋白与MALS/CASK相关联，这表明该复合体将突触前释放机制与活性区相连接，从而调节神经递质释放。
