Chen D F, Schneider G E, Martinou J C, Tonegawa S
Howard Hughes Medical Institute, Center for Learning and Memory, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139, USA.
Nature. 1997 Jan 30;385(6615):434-9. doi: 10.1038/385434a0.
Most neurons of the mammalian central nervous system (CNS) lose the ability to regenerate severed axons in vivo after a certain point in development. At least part of this loss in regenerative potential is intrinsic to neurons. Although embryonic retinal ganglion cells (RGCs) can grow axons into tectum of any age, most RGCs from older animals fail to extend axons into CNS tissue derived from donors of any age, including the embryonic tectum. Here we report that the proto-oncogene bcl-2 plays a key role in this developmental change by promoting the growth and regeneration of retinal axons. This effect does not seem to be an indirect consequence of its well-known anti-apoptotic activity. Another anti-apoptotic drug, ZVAD, supported neuronal survival but did not promote axon regeneration in culture. This finding could lead to new strategies for the treatment of injuries to the CNS.
哺乳动物中枢神经系统（CNS）的大多数神经元在发育的某个阶段后失去了在体内再生切断轴突的能力。这种再生潜力的丧失至少部分是神经元固有的。虽然胚胎视网膜神经节细胞（RGCs）可以将轴突生长到任何年龄的视盖中，但来自成年动物的大多数RGCs无法将轴突延伸到来自任何年龄供体的CNS组织中，包括胚胎视盖。在这里，我们报告原癌基因bcl-2通过促进视网膜轴突的生长和再生在这种发育变化中起关键作用。这种作用似乎不是其众所周知的抗凋亡活性的间接结果。另一种抗凋亡药物ZVAD可支持神经元存活，但在培养中不促进轴突再生。这一发现可能会导致治疗CNS损伤的新策略。
