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首页> 外文期刊>The European Journal of Neuroscience >Bi-directional regulation of postsynaptic cortactin distribution by BDNF and NMDA receptor activity.
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Bi-directional regulation of postsynaptic cortactin distribution by BDNF and NMDA receptor activity.

机译：BDNF和NMDA受体活性对突触后皮质激素分布的双向调节。

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Abstract Cortactin is an F-actin-associated protein which interacts with the postsynaptic scaffolding protein Shank at the SH3 domain and is localized within the dendritic spine in the mouse neuron. Green fluorescent protein (GFP)-based time-lapse imaging revealed cortactin redistribution from dendritic cytoplasm to postsynaptic sites by application of brain-derived neurotrophic factor (BDNF). This response was mediated by mitogen-activated protein (MAP) kinase activation and was dependent on the C-terminal SH3 domain. In contrast, activation of N-methyl-D-aspartate (NMDA) receptors induced loss of cortactin from postsynaptic sites. This NMDA-dependent redistribution was blocked by an Src family kinase inhibitor. Conversely, increasing Src family kinase activity induced cortactin phosphorylation and loss of cortactin from the postsynaptic sites. Finally, blocking of endogenous BDNF reduced the amount of cortactin at the postsynaptic sites and an NMDA receptor antagonist prevented this reduction. These results indicate the importance of counterbalance between BDNF and NMDA receptor-mediated signalling in the reorganization of the postsynaptic actin cytoskeleton during neuronal development.
机译：摘要Cortactin是一种F-肌动蛋白相关蛋白，在SH3结构域与突触后支架蛋白Shank相互作用，位于小鼠神经元的树突棘中。基于绿色荧光蛋白（GFP）的延时成像显示，通过应用脑源性神经营养因子（BDNF），皮质激素从树突状细胞质重新分布到突触后部位。此反应是由有丝分裂原激活蛋白（MAP）激酶激活介导的，并且依赖于C末端SH3结构域。相反，N-甲基-D-天冬氨酸（NMDA）受体的激活诱导了突触后位点中的cortactin的损失。依赖NMDA的重新分布被Src家族激酶抑制剂阻断。相反，增加的Src家族激酶活性会诱导皮质激素的磷酸化和皮质激素从突触后位点的损失。最后，内源性BDNF的阻断减少了突触后位点的皮质激素含量，而NMDA受体拮抗剂阻止了这种减少。这些结果表明，在神经元发育过程中，BDNF和NMDA受体介导的信号传导之间的平衡平衡在突触后肌动蛋白细胞骨架重组中的重要性。

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