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首页> 外文期刊>The European Journal of Neuroscience >Transient decrease in F-actin may be necessary for translocation of proteins into dendritic spines.
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Transient decrease in F-actin may be necessary for translocation of proteins into dendritic spines.

机译：F-肌动蛋白的短暂降低对于蛋白质易位到树突棘中可能是必需的。

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It remains poorly understood as to how newly synthesized proteins that are required to act at specific synapses are translocated into only selected subsets of potentiated dendritic spines. Here, we report that F-actin, a major component of the skeletal structure of dendritic spines, may contribute to the regulation of synaptic specificity of protein translocation. We found that the stabilization of F-actin blocked the translocation of GFP-CaMKII and inhibited the diffusion of 3-kDa dextran into spines (in 2-3 weeks cultures). Neuronal activation in hippocampal slices and cultured neurons led to an increase in the activation (decrease in the phosphorylation) of the actin depolymerization factor, cofilin, and a decrease in F-actin. Furthermore, the induction of long-term potentiation by tetanic stimulation induced local transient depolymerization of F-actin both in vivo and in hippocampal slices (8-10 weeks), and this local F-actin depolymerization was blocked by APV, a N-methyl-D-aspartate (NMDA) receptor antagonist. These results suggest that F-actin may play a role in synaptic specificity by allowing protein translocation into only potentiated spines, gated through its depolymerization, which is probably triggered by the activation of NMDA receptors.
机译：关于如何作用于特定突触的新合成蛋白质如何仅转移到增强的树突棘的选定子集中，仍然知之甚少。在这里，我们报告F-肌动蛋白，树突棘的骨骼结构的主要组成部分，可能有助于调节蛋白转运的突触特异性。我们发现，F-肌动蛋白的稳定作用阻止了GFP-CaMKII的转运，并抑制了3-kDa葡聚糖向棘的扩散（在2-3周的培养中）。海马切片和培养的神经元中的神经元激活导致肌动蛋白解聚因子，cofilin的激活增加（磷酸化降低），F-肌动蛋白减少。此外，强直性刺激诱导的长时程增强在体内和海马切片中均引起F-肌动蛋白的局部瞬时解聚（8-10周），而局部F-肌动蛋白的解聚被APV（一种N-甲基）阻断-D-天冬氨酸（NMDA）受体拮抗剂。这些结果表明，F-肌动蛋白可能通过允许蛋白质易位进入仅通过增强的脱模板作用的增强的棘突而可能在突触特异性中起作用，这可能是由NMDA受体的激活触发的。

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