Johnson E M, Chang J Y, Koike T, Martin D P
Department of Pharmacology, Washington University Medical School, St. Louis, MO 63110.
Neurobiol Aging. 1989 Sep-Oct;10(5):549-52; discussion 552-3. doi: 10.1016/0197-4580(89)90127-9.
In this commentary we present circumstantial evidence which supports the hypothesis that neuronal death produced by trophic factor deprivation (i.e., axotomy, target loss, etc.) is not a passive process resulting from a loss of trophic stimulation. Rather, we suggest that it is due to the activation of an endogenous "suicide program" requiring mRNA and protein synthesis. The possible mechanistic relationship of neuronal death to death of other cell types, both in the developing and adult organism, is discussed. If this hypothesis of active death is true, then loss of transcriptional control of this program may be involved in neuronal attrition in aging or neurodegenerative disease.
在本评论中，我们提供了间接证据，支持以下假说：由营养因子剥夺（即轴突切断、靶标丧失等）导致的神经元死亡并非营养刺激丧失所导致的被动过程。相反，我们认为这是由于一种需要mRNA和蛋白质合成的内源性“自杀程序”被激活所致。本文还讨论了在发育中和成年生物体中，神经元死亡与其他细胞类型死亡之间可能的机制关系。如果这种主动死亡的假说是正确的，那么该程序转录控制的丧失可能与衰老或神经退行性疾病中的神经元损耗有关。
