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Arp2/3 Is Required for Axonal Arbor Terminal Retraction in Cerebellar Granule Neurons
Neurochemical Journal ( IF 0.5 ) Pub Date : 2020-03-31 , DOI: 10.1134/s1819712420010109
T. Ikeno , Y. Konishi

Abstract

Although selective pruning of subsets of branches is a key step for axonal remodeling, the underlying mechanisms have not fully elucidated. We have reported that the retraction rate of axonal arbor is higher in the terminals, where less kinesin is sorted, and inhibiting actin turnover by treatment with latrunculin A prevented retraction in such terminals. In the present study, we investigated the effects of pharmacological inhibitors for the regulators of actin polymerization/destabilization on the elongation and retraction of arbor terminals in cerebellar granule neurons. Inhibition of an actin nucleator Arp2/3 with CK-666 or CK-869 inhibited the retraction of arbor terminals. However, inhibitors for PAK/LIMK, upstream signaling of ADF/cofilin, reduced the elongation rate but not the retraction rate. A photoconversion analysis revealed that turnover of F-actin at the tip of the axonal terminal is faster in the presence of the Arp2/3 inhibitor compared with the control and neurons treated with the LIMK inhibitor. Our results indicate the important role of Arp2/3 for the retraction of axonal arbor terminals in cerebellar granule neurons.


中文翻译:

小脑颗粒神经元轴突乔木末端缩回需要Arp2 / 3。

摘要

尽管选择性修剪分支的子集是轴突重塑的关键步骤,但其潜在机制尚未完全阐明。我们已经报道,轴索柄的缩回率在终端中较高,其中驱动蛋白的分选较少,并且通过用拉曲霉素A治疗抑制肌动蛋白周转防止了在这种终端中的缩回。在本研究中,我们研究了肌动蛋白聚合/去稳定作用调节剂的药理抑制剂对小脑颗粒神经元柄轴末端伸长和收缩的影响。用CK-666或CK-869抑制肌动蛋白成核剂Arp2 / 3抑制了乔木末端的缩回。但是,PAK / LIMK抑制剂,ADF / cofilin的上游信号传导降低了伸长率,但没有降低缩回率。光转换分析显示,与对照组和用LIMK抑制剂治疗的神经元相比,在Arp2 / 3抑制剂存在下,轴突末端F-肌动蛋白的更新更快。我们的结果表明Arp2 / 3在小脑颗粒神经元的轴突乔木末端的撤回中的重要作用。
更新日期:2020-03-31
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