Hier D B, Arnason B G, Young M
Proc Natl Acad Sci U S A. 1972 Aug;69(8):2268-72. doi: 10.1073/pnas.69.8.2268.
In this study, explanted chick-embryo sensory ganglia were treated with nerve growth factor, and cellular concentrations of neurotubule protein were measured chemically by a colchicine-binding assay. Even after brief time periods, ganglia treated with growth factor were enriched in neurotubule protein, as compared with untreated (control) ganglia. Furthermore, studies with ganglia treated with both vincristine and growth factor demonstrated that neurotubule protein synthesis can occur even though neurite outgrowth is abolished. Several lines of evidence indicate that the growth factor stimulates de novo synthesis of neurotubule subunit protein, and that this effect precedes neurite extension. Like nerve growth factor, dibutyryl cyclic AMP also stimulates neurite outgrowth from embryonic sensory ganglia, yet it does not increase neurotubule protein levels. Available information suggests that the ability of growth factor to elicit rapid neurite outgrowth is closely related to its ability to increase cellular neurotubule levels. Cyclic AMP appears to stimulate neurite outgrowth by a different mechanism.
在本研究中，将取出的鸡胚感觉神经节用神经生长因子处理，并用秋水仙碱结合试验化学测定神经微管蛋白的细胞浓度。即使在短时间后，与未处理（对照）的神经节相比，用生长因子处理的神经节中神经微管蛋白也有所富集。此外，对用长春新碱和生长因子处理的神经节的研究表明，即使神经突生长被阻断，神经微管蛋白的合成仍可发生。几条证据表明，生长因子刺激神经微管亚基蛋白的从头合成，且这种作用先于神经突延伸。与神经生长因子一样，二丁酰环磷腺苷也刺激胚胎感觉神经节的神经突生长，但它不会增加神经微管蛋白水平。现有信息表明，生长因子引发快速神经突生长的能力与其增加细胞神经微管水平的能力密切相关。环磷腺苷似乎通过不同机制刺激神经突生长。
