Ultrastructural differences during embryonic cell death in normal and peripherally deprived ciliary ganglia.
Ultrastructural differences during embryonic cell death in normal and peripherally deprived ciliary ganglia.
复制标题
DOI：
10.1083/jcb.68.2.339
复制
发表时间：
1976-02
期刊：
影响因子：
--
通讯作者：
Landmesser L
中科院分区：
文献类型：
--
作者：
Pilar G;Landmesser L
为了更好地了解该系统中细胞死亡的机制，在鸡胚睫状神经节中对正常发生的神经元死亡和预先去除外周靶器官所带来的神经元死亡进行了超微结构研究。在细胞死亡之前，正常神经节中的所有神经元都发育出一个组织良好的粗面内质网（RER），这与周围突触的形成相吻合。没有一个被剥夺外周神经元经历这种变化，这表明与外周神经元的一些相互作用，可能是突触的形成，触发了它们进入分泌状态。外周剥夺神经元的细胞死亡信号核的变化，然后从多聚核糖体和粗面内质网释放核糖体，并推测蛋白质合成的停止。相反，正常细胞死亡是由粗面内质网扩张引起的，最终细胞质破裂，核变化只是次要的。这表明，未能形成或维持外周突触可能会导致传输相关蛋白的积累，随之而来的脑池扩张，并最终导致细胞死亡。
Normally occurring neuron death and that brought about by prior removal of the peripheral target organ was studied ultrastructurally in embryonic chick ciliary ganglion in order to better understand the mechanism of cell death in this system. Before the period of cell death, all neurons in the normal ganglion developed a well-organized rough endoplasmic reticulum (RER) which coincided with peripheral synapse formation. None of the peripherally deprived neurons underwent this change, suggesting that some interaction with the periphery, possibly synapse formation, triggered them into the secretory state. Cell death in peripherally deprived neurons was signalled by nuclear changes followed by freeing of ribosomes from polysomes and RER and presumably cessation of protein synthesis. In contrast, normal cell death was brought about by dilation of the RER with eventual cytoplasmic disruption, nuclear changes appearing only secondarily. It is suggested that failure to form or maintain peripheral synapses could result in the accumulation of transmission-related proteins with consequent cisternal dilation, and eventual cell death.