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在程序性细胞死亡(凋亡)导致神经元胞体破坏后,神经突仍可存活。

Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis).

作者信息

Deckwerth T L, Johnson E M

机构信息

Washington University School of Medicine, Department of Molecular Biology and Pharmacology, St. Louis, Missouri 63110.

出版信息

Dev Biol. 1994 Sep;165(1):63-72. doi: 10.1006/dbio.1994.1234.

Abstract

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 (Wld6) 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 occurring 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.

摘要

在神经系统发育过程中,会发生广泛的程序性神经元死亡,这一过程受神经营养因子调控。无一例外,由于营养因子剥夺导致的神经元胞体变性和死亡,都会伴随着神经突的同时变性。通过研究交感神经元在被剥夺其生理性神经营养因子神经生长因子后的变性情况,我们发现纯合突变C57BL/Ola小鼠所表达的“慢沃勒变性”等位基因(Wld6),通过选择性地显著延迟神经突崩解的起始,改变了程序性神经元死亡的正常时间进程。相比之下,影响神经元胞体的变性事件并未改变:胞体萎缩、细胞核的凋亡崩解、死亡的发生以及活力的丧失均正常出现。胞体死亡后残留的无核神经突具有完整的质膜,代谢活跃,并且其物理完整性需要活跃的代谢。我们认为,发育过程中发生的神经元死亡期间神经突的变性,是由局限于神经突的事件所控制的,并且独立于神经元胞体自主发生。此外,胞体的程序性神经元死亡独立于变性神经突所施加的任何影响而进行。

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