Xue Mingshan, Stradomska Alicja, Chen Hongmei, Brose Nils, Zhang Weiqi, Rosenmund Christian, Reim Kerstin
Departments of Neuroscience and Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Proc Natl Acad Sci U S A. 2008 Jun 3;105(22):7875-80. doi: 10.1073/pnas.0803012105. Epub 2008 May 27.
Complexins (Cplxs) are key regulators of synaptic exocytosis, but whether they act as facilitators or inhibitors is currently being disputed controversially. We show that genetic deletion of all Cplxs expressed in the mouse brain causes a reduction in Ca(2+)-triggered and spontaneous neurotransmitter release at both excitatory and inhibitory synapses. Our results demonstrate that at mammalian central nervous system synapses, Cplxs facilitate neurotransmitter release and do not simply act as inhibitory clamps of the synaptic vesicle fusion machinery.
复合体蛋白（Complexins，Cplxs）是突触囊泡外排的关键调节因子，但它们究竟是起促进作用还是抑制作用目前仍存在争议。我们发现，小鼠大脑中表达的所有复合体蛋白基因敲除后，兴奋性和抑制性突触处由钙离子触发的以及自发的神经递质释放均减少。我们的结果表明，在哺乳动物中枢神经系统突触中，复合体蛋白促进神经递质释放，而不仅仅是作为突触囊泡融合机制的抑制钳。
