Pilar G, Landmesser L
J Cell Biol. 1976 Feb;68(2):339-56. doi: 10.1083/jcb.68.2.339.
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.
为了更好地理解该系统中细胞死亡的机制,对正常发生的神经元死亡以及由先前去除外周靶器官导致的神经元死亡进行了超微结构研究,研究对象是胚胎期鸡睫状神经节。在细胞死亡期之前,正常神经节中的所有神经元都发育出了组织良好的粗面内质网(RER),这与外周突触形成同时发生。所有外周剥夺的神经元均未发生这种变化,这表明与外周的某些相互作用,可能是突触形成,促使它们进入分泌状态。外周剥夺神经元的细胞死亡以核变化为信号,随后核糖体从多核糖体和RER中释放出来,推测蛋白质合成停止。相比之下,正常细胞死亡是由RER扩张最终导致细胞质破坏引起的,核变化只是其次出现。有人提出,未能形成或维持外周突触可能导致与传递相关的蛋白质积累,从而导致潴泡扩张,最终导致细胞死亡。