Finklestein S P, Apostolides P J, Caday C G, Philips M F, Perrone-Bizzozero N I, Benowitz L I
Mailman Research Center, McLean Hospital, Belmont, MA 02178.
Brain Res. 1988 May 17;448(2):346-50. doi: 10.1016/0006-8993(88)91274-7.
Unlike mammals, lower vertebrates retain the capacity to regenerate damaged central nervous system (CNS) pathways throughout life. In previous studies, we have used the goldfish optic nerve (ON) as a model for CNS regeneration, and found that the injured goldfish ON selectively secretes a factor that promotes process outgrowth of cultured neurons, including neurons of the developing rodent CNS. In the current study, we found that a factor similarly obtained from the injured goldfish ON also has potent outgrowth-promoting effects on cerebrocortical neurons of the fetal human brain, and that these effects are dependent on the age of fetal neurons. This factor appeared to be a protein of mol. wt. greater than 12,000, and was associated with a distinctive morphology of neurite outgrowth. The neurite-promoting factor from the injured goldfish ON may be homologous to factors within the developing human brain.
与哺乳动物不同,低等脊椎动物终生都保留着再生受损中枢神经系统(CNS)通路的能力。在之前的研究中,我们使用金鱼视神经(ON)作为中枢神经系统再生的模型,并发现受伤的金鱼视神经选择性地分泌一种促进培养神经元(包括发育中的啮齿动物中枢神经系统的神经元)轴突生长的因子。在当前的研究中,我们发现从受伤的金鱼视神经中类似地获得的一种因子对胎儿人脑的大脑皮质神经元也有强大的促生长作用,并且这些作用取决于胎儿神经元的年龄。这种因子似乎是一种分子量大于12000的蛋白质,并且与轴突生长的独特形态有关。来自受伤金鱼视神经的轴突促进因子可能与发育中的人类大脑中的因子同源。