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去除神经输入后成熟电器官中肌源性蛋白的重新表达。

Reexpression of myogenic proteins in mature electric organ after removal of neural input.

作者信息

Unguez G A, Zakon H H

机构信息

Department of Zoology and Institute for Neuroscience, University of Texas, Austin, Texas 78712, USA.

出版信息

J Neurosci. 1998 Dec 1;18(23):9924-35. doi: 10.1523/JNEUROSCI.18-23-09924.1998.

Abstract

The electric organ (EO) of the weakly electric fish Sternopygus macrurus derives from striated myofibers that fuse and suppress many muscle properties. Mature electrocytes are larger than muscle fibers, do not contain sarcomeres, or express myosin heavy chain (MHC) or tropomyosin. Furthermore, electrocytes express keratin, a protein not expressed in muscle. In S. macrurus the EO is driven continuously at frequencies higher than those of the intermittently active skeletal muscle. The extent to which differences in EO and muscle phenotype are accounted for by activity patterns, or innervation per se, was determined by assessing the expression of MHC, tropomyosin, and keratin 2 and 5 weeks after the elimination of (1) activity patterns by spinal transection or (2) all synaptic input by denervation. Immunohistochemical analyses showed no changes in muscle fiber phenotypes after either experimental treatment. In contrast, the keratin-positive electrocytes revealed an upregulation of MHC and tropomyosin. Nearly one-third of all electrocytes expressed MHC (35%) and tropomyosin (25%) 2 weeks after spinal transection, whereas approximately two-thirds (61%) expressed MHC 2 weeks after denervation. After 5 weeks of denervation or spinal transection, all electrocytes contained MHC and tropomyosin. Newly formed sarcomere clusters also were observed in denervated electrocytes. The MHC expressed in electrocytes corresponded to that present in a select population of muscle fibers, i.e., type II fibers. Thus, the elimination of electrical activity or all synaptic input resulted in a partial reversal of the electrocyte phenotype to an earlier developmental stage of its myogenic lineage.

摘要

弱电鱼大吻电鳗的发电器官(EO)源自融合并抑制多种肌肉特性的横纹肌纤维。成熟的电细胞比肌纤维大,不含肌节,也不表达肌球蛋白重链(MHC)或原肌球蛋白。此外,电细胞表达角蛋白,一种在肌肉中不表达的蛋白质。在大吻电鳗中,EO以高于间歇性活动的骨骼肌的频率持续驱动。通过评估在消除(1)通过脊髓横断消除活动模式或(2)通过去神经支配消除所有突触输入后2周和5周时MHC、原肌球蛋白和角蛋白的表达,确定了EO和肌肉表型差异在多大程度上是由活动模式或神经支配本身造成的。免疫组织化学分析表明,两种实验处理后肌纤维表型均无变化。相比之下,角蛋白阳性的电细胞显示MHC和原肌球蛋白上调。脊髓横断后2周,近三分之一的电细胞表达MHC(35%)和原肌球蛋白(25%),而去神经支配后2周,约三分之二(61%)的电细胞表达MHC。去神经支配或脊髓横断5周后,所有电细胞都含有MHC和原肌球蛋白。在去神经支配的电细胞中也观察到新形成的肌节簇。电细胞中表达的MHC与特定群体的肌纤维(即II型纤维)中存在的MHC相对应。因此,消除电活动或所有突触输入导致电细胞表型部分逆转到其肌源性谱系的早期发育阶段。

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