NEURITES CAN REMAIN VIABLE AFTER DESTRUCTION OF THE NEURONAL SOMA BY PROGRAMMED CELL-DEATH (APOPTOSIS)
NEURITES CAN REMAIN VIABLE AFTER DESTRUCTION OF THE NEURONAL SOMA BY PROGRAMMED CELL-DEATH (APOPTOSIS)
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DOI：
10.1006/dbio.1994.1234
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发表时间：
1994-09-01
影响因子：
2.7
通讯作者：
JOHNSON, EM
中科院分区：
文献类型：
--
作者：
DECKWERTH, TL;JOHNSON, EM
在神经系统发育过程中，广泛的程序性神经元死亡是由神经营养因子调控的。由于营养因子剥夺而导致的神经元体变性和死亡总是伴随着神经突的变性。通过检测生理营养因子神经生长因子被剥夺后交感神经元的变性，我们发现纯合突变体C57BL/Ola小鼠表达的“慢沃勒氏变性”等位基因（Wld(s)）通过选择性地显著延缓神经突崩解的发生，改变了程序性神经元死亡的正常时间进程。相反，影响神经元胞体的退行性事件没有改变：胞体萎缩、细胞核凋亡解体、死亡承诺和生存能力丧失正常发生。体细胞死亡后留下的无核神经突具有完整的质膜，具有代谢活性，需要积极的代谢才能保持身体的完整性。我们认为，在发育发生的神经元死亡过程中，神经突的退化是由局限于神经突的事件控制的，并从神经元体自主发生。此外，体细胞的程序性神经元死亡独立于任何退化的神经突施加的影响。(C) 1994学术出版社，Inc.
During the development of the nervous system extensive programmed neuronal death occurs that is regulated by neurotrophic factors. Invariably, degeneration and death of the neuronal soma as a result of trophic factor deprivation is accompanied by concurrent degeneration of the neurites. By examining the degeneration of sympathetic neurons after deprivation of their physiological trophic factor nerve growth factor, we show that the ''slow Wallerian degeneration'' allele (Wld(s)) expressed by homozygous mutant C57BL/Ola mice alters the normal time course of programmed neuronal death by selectively and dramatically delaying the onset of neurite disintegration. In contrast, degenerative events affecting the neuronal soma are not altered: Atrophy of the soma, apoptotic disintegration of the nucleus, commitment to die, and loss of viability occur normally. The enucleate neurites remaining after death of the soma have an intact plasma membrane, are metabolically active, and require an active metabolism for physical integrity. We suggest that the degeneration of neurites during developmentally occuring neuronal death is controlled by events confined to the neurites and occurs autonomously from the neuronal soma. Furthermore, programmed neuronal death of the soma proceeds independent from any influence exerted by degenerating neurites. (C) 1994 Academic Press, Inc.