Itoh T, Sobue G, Yasuda T, Kimata K, Mitsuma T, Takahashi A
Department of Neurology, Nagoya University School of Medicine, Japan.
Neurobiol Aging. 1993 Mar-Apr;14(2):167-76. doi: 10.1016/0197-4580(93)90093-q.
We previously established a single-neuron culture system to analyze the primary effects of neurotrophic factors and reported that NGF promoted neurite extension in young adult (4- to 6-month-old) rat dorsal root ganglion (DRG) neurons by promoting neurite arborization. In this study, we demonstrated that the effects of NGF on neurite regeneration in DRG neurons was well preserved in aged rats (20- to 24-month-old and 33-month-old). NGF did not increase the percent process-bearing neurons in aged rats, which indicated that neuronal survival was not promoted by NGF, but it significantly enhanced the number of branching points, total neurite length, and soma size in aged neurons. These effects of NGF on neurite geometry tended to be reduced to some extent in aged neurons and the initiation of neurite-outgrowth in aged neurons was also delayed as compared with young adult neurons. NGF-responsive subpopulation of neurons, found in the entire range of neuronal size, were preserved in aged rats. These findings indicate that NGF could play an important role in regeneration of injured DRG neurons of aged animals.
我们之前建立了一种单神经元培养系统来分析神经营养因子的主要作用,并报告称神经生长因子(NGF)通过促进神经突分支来促进成年早期(4至6个月大)大鼠背根神经节(DRG)神经元的神经突延伸。在本研究中,我们证明了NGF对老年大鼠(20至24个月大以及33个月大)DRG神经元神经突再生的作用得到了很好的保留。NGF并未增加老年大鼠中具有突起的神经元的比例,这表明NGF并未促进神经元存活,但它显著增加了老年神经元的分支点数量、总神经突长度和胞体大小。与成年早期神经元相比,NGF对老年神经元神经突形态的这些作用在一定程度上有所减弱,并且老年神经元神经突生长的起始也延迟了。在整个神经元大小范围内发现的对NGF有反应的神经元亚群在老年大鼠中得以保留。这些发现表明,NGF可能在老年动物受损DRG神经元的再生中发挥重要作用。