运动神经元损伤致肌萎缩的相关机制研究进展  

Progress on the mechanism of muscle atrophy induced by motor neuron injury

作　　者：杨胜波[1] 

机构地区：[1]遵义医学院解剖学教研室,贵州遵义563099

出　　处：《遵义医学院学报》2015年第6期560-566,共7页Journal of Zunyi Medical University

基　　金：国家自然科学基金资助项目(NO:31540031);贵州省联合基金资助项目(NO:黔科合LH字[2015]7528)

摘　　要：神经系统控制骨骼肌依赖于运动神经元的电活动和神经末梢释放可溶性因子。一旦神经元受损,则发生快速肌萎缩。近年来研究发现,失神经支配的肌纤维萎缩前,肌细胞膜通透性增加、电活动减少,与连接蛋白形成的半通道重新表达有关;一些抑制连接蛋白表达的细胞外信号分子参与了抑制肌萎缩的信号通路;肌微循环和多种神经营养因子参与肌营养作用。为此,本文围绕近来相关文献报道作一综述,以期更好地理解神经损伤致肌萎缩的机制,为防治运动神经元损伤后肌萎缩设计合理方案提供资料。The control skeletal muscle by the neural system depends on the electrical activity of motor neurons and the release of soluble factors from nerve terminals.Once the neurons are damaged,the rapid muscle atrophy occurs.Recently,it was found that the increased sarcolemmal permeability and the decreased electrical activity of the neurons were related to the de novo expression of connexin hemichannels,all of which happen before the denervated skeletal muscle fibers appear atrophy;some of the extracellular signal molecules that inhibit the expression of the connexin proteins were involved in the inhibition of the signal transduction pathway of muscle atrophy;the muscle microcirculation and many neurotrophic factors were also involved in the muscular atrophy.To this end,this article reviews the current status of these studies in order to better understand the mechanism of muscle atrophy caused by nerve injury and to provide information on the design of a reasonable treatment plan for the prevention and treatment of muscle atrophy after motor neuron injury.

关 键 词：运动神经元损伤 肌萎缩 电活动 神经营养因子 

分 类 号：R322[医药卫生—人体解剖和组织胚胎学]