Maletic-Savatic M, Malinow R
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
J Neurosci. 1998 Sep 1;18(17):6803-13. doi: 10.1523/JNEUROSCI.18-17-06803.1998.
Exocytosis is a widely observed cellular mechanism for delivering transmembrane proteins to the cell surface and releasing signaling molecules into the extracellular space. Calcium-evoked exocytosis, traditionally thought to be restricted to presynaptic specializations in neurons, has been described recently in many cells. Here, calcium-evoked dendritic exocytosis (CEDE) is visualized in living cultured hippocampal neurons. Organelles that undergo CEDE are in somata, dendrites, and perisynaptic regions, identified by using immunocytochemistry and correlative light and electron microscopy. CEDE is regulated developmentally: neurons <9 d in vitro do not show CEDE. In addition, CEDE is blocked by tetanus toxin, an inhibitor of regulated exocytosis, and nocodazole, an inhibitor of microtubule polymerization. Organelles that undergo CEDE often are found on the base of spines, putative sites of synaptic plasticity. CEDE therefore could be involved in structural and functional modification of spines and could play a role in synaptic plasticity, where it might involve changes in receptor/channel density, release of active compounds having effect on pre- and postsynaptic function, and/or growth of synaptic structures.
胞吐作用是一种广泛存在的细胞机制,用于将跨膜蛋白递送至细胞表面,并将信号分子释放到细胞外空间。钙触发的胞吐作用,传统上认为仅限于神经元的突触前特化结构,最近在许多细胞中都有报道。在此,在培养的活海马神经元中观察到了钙触发的树突胞吐作用(CEDE)。通过免疫细胞化学以及相关的光学和电子显微镜鉴定,发现经历CEDE的细胞器存在于胞体、树突和突触周围区域。CEDE受发育调控:体外培养9天以内的神经元未表现出CEDE。此外,CEDE被破伤风毒素(一种调节性胞吐作用的抑制剂)和诺考达唑(一种微管聚合作用的抑制剂)所阻断。经历CEDE的细胞器常位于棘突基部,这是突触可塑性的假定部位。因此,CEDE可能参与棘突的结构和功能修饰,并可能在突触可塑性中发挥作用,这可能涉及受体/通道密度的变化、对突触前和突触后功能有影响的活性化合物的释放,和/或突触结构的生长。