Suppr超能文献

[作为蝎毒靶点的莫氏神经元的类桥粒连接]

[Desmosome-like contacts of Mauthner neurons as targets of scorpion venom].

作者信息

Mikheeva I B, Tiras N R, Moshkov D A, Pashkov V I, Grishin E V

机构信息

Department of Cytotechnology, Pushchino State University.

出版信息

Tsitologiia. 2000;42(7):635-46.

Abstract

Desmosome-like contacts (DLC) in afferent chemical synapses of the Mauthner cells (MC) were investigated after application of low and high molecular mass peptide fractions 6 and 9, correspondingly, from the Central Asiatic black scorpion Orthochirus scrobiculosus. Besides, the DLC were examined in condition of a training induced morpho-functional stability of the MC (adaptation) mediated by transformation of actin monomers into polymers. In addition, the structure of DLC was studied after cytochalasin application which disrupts F-actin. Fraction 6 was shown to increase the length of DLC and osmiophily of fibrous material. Similar changes in DLC were caused by adaptation. Fraction 9 decreased the osmiophily of the fibrous material, made DLC asymmetric, but did not influence their length. Similar changes in DLC were seen also after cytochalasin D application. Taking into account our previous data on the role of F-actin in the MC functioning, which were obtained following specific pharmacological treatments, the similarity of ultrastructural changes in DLC after both adaptation and fraction 6 application, on the one hand, and after both cytochalasin D and fraction 9 application, on the other one, enabled us to suggest that these fractions may contain peptides able to exert influence of the actin cytoskeleton.

摘要

分别应用来自中亚黑蝎直额蝎的低分子量和高分子量肽组分6和9后,对Mauthner细胞(MC)传入化学突触中的类桥粒接触(DLC)进行了研究。此外,在由肌动蛋白单体转化为聚合物介导的MC训练诱导形态功能稳定性(适应)的条件下,对DLC进行了检查。另外,在应用破坏F-肌动蛋白的细胞松弛素后,研究了DLC的结构。结果显示,组分6增加了DLC的长度和纤维材料的嗜锇性。适应也导致DLC发生类似变化。组分9降低了纤维材料的嗜锇性,使DLC不对称,但不影响其长度。应用细胞松弛素D后,DLC也出现类似变化。考虑到我们之前通过特定药理学处理获得的关于F-肌动蛋白在MC功能中作用的数据,一方面,适应和应用组分6后DLC超微结构变化的相似性,另一方面,应用细胞松弛素D和组分9后DLC超微结构变化的相似性,使我们能够推测这些组分可能含有能够影响肌动蛋白细胞骨架的肽。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验