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螺旋神经节指令神经元中乙酰胆碱诱导内向电流的类习惯化降低:微管运动蛋白的作用

Habituation-Like Decrease of Acetylcholine-Induced Inward Current in Helix Command Neurons: Role of Microtubule Motor Proteins.

作者信息

Vasil'yeva Natal'ya A, Murzina Galina B, Pivovarov Arkady S

机构信息

Department of Higher Nervous Activity, Faculty of Biology, Moscow Lomonosov State University, Leninskie Gory dom 1, Stroenie 12, Moscow, 119991, Russia.

出版信息

Cell Mol Neurobiol. 2015 Jul;35(5):703-12. doi: 10.1007/s10571-015-0165-y. Epub 2015 Feb 17.

DOI:10.1007/s10571-015-0165-y
PMID:25687906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11486294/
Abstract

The role of kinesin and dynein microtubule-associated molecular motors in the cellular mechanism of depression of acetylcholine-induced inward chloride current (ACh-current) was examined in command neurons of land snails (Helix lucorum) in response to repeated applications of ACh to neuronal soma. This pharmacological stimulation imitated the protocol of tactile stimulation evoking behavioural habituation of the defensive reaction. In this system, a dynein inhibitor (erythro-9-(2-hydroxy-3-nonyl)adenine, 50 µM) decreased the ACh-current depression rate. Kinesin Eg5 inhibitors (Eg5 inhibitor III, 10 µM and Eg5 inhibitor V, trans-24, 15 µM) reduced the degree of current depression, and Eg5 inhibitor V also reduced the initial rate of depression. The results of electrophysiological experiments in combination with mathematical modelling provided evidence of the participation of dyneins and kinesin Eg5 proteins in the radial transport of acetylcholine receptors in command neurons of H. lucorum in the cellular analogue of habituation. Furthermore, these results suggest that the reciprocal interaction between dynein and kinesin proteins located on the same vesicle can lead to reverse their usual direction of transport (dyneins-in exocytosis and kinesin Eg5-in endocytosis).

摘要

在陆地蜗牛(光亮蜗牛)的指令神经元中,研究了驱动蛋白和动力蛋白这两种微管相关分子马达在乙酰胆碱诱导的内向氯离子电流(ACh电流)抑制的细胞机制中的作用,该研究通过向神经元胞体反复施加乙酰胆碱来进行。这种药理学刺激模拟了诱发防御反应行为习惯化的触觉刺激方案。在这个系统中,一种动力蛋白抑制剂(赤藓红-9-(2-羟基-3-壬基)腺嘌呤,50 μM)降低了ACh电流的抑制率。驱动蛋白Eg5抑制剂(Eg5抑制剂III,10 μM和Eg5抑制剂V,反式-24,15 μM)降低了电流抑制程度,并且Eg5抑制剂V还降低了初始抑制率。电生理实验结果与数学建模相结合,为动力蛋白和驱动蛋白Eg5蛋白参与光亮蜗牛指令神经元中乙酰胆碱受体在习惯化细胞类似物中的径向运输提供了证据。此外,这些结果表明,位于同一囊泡上的动力蛋白和驱动蛋白之间的相互作用可能导致它们通常的运输方向反转(动力蛋白-胞吐作用中向内,驱动蛋白Eg5-内吞作用中向内)。

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