Hendry I A
Brain Res. 1975 Aug 22;94(1):87-97. doi: 10.1016/0006-8993(75)90879-3.
Division of the axons of adrenergic neurones by crushing the postganglionic nerve trunks of rat superior cervical ganglia (SCG) at 6 days of age resulted in a permanent atrophy of the SCG reflected by a persistent decrease in the total protein content and in the activities of the enzymes tyrosine hydroxylase and DOPA decarboxylase. Administration of nerve growth factor (NGF) to rats with unilateral axotomy at a dose of 10 mug/g/day for the period 7-21 days of age resulted in hypertrophy of both normal and axotomised SCG. There was a progressive rise in the total protein content and in the activities of the two enzymes till the end of the treatment period in both SCG. After treatment ceased there was a progressive fall in the total protein content and activities of the two enzymes reaching a stable level after 4 weeks. The level reached for treated unoperated SCG remained elevated when compared to untreated control SCG. Axotomised treated SCG had approximately the same biochemical parameters as untreated control SCG and very much elevated over untreated axotomised SCG. These final levels persisted for at least 56 days after treatment had ceased. Animals showed a persistent ptosis after axotomy at 6 days of age but treatment with NGF resulted in a functional recovery by 11 weeks of age. It is suggested that there is normally a retrograde transfer of a factor durind development from the target cell to the perikarya of the neurone permitting survival if the appropriate connections are made. Failure to make such a contact results in cedd death. The cell death occurring normally, and the cell death resulting from axotomy, can both be prevented by NGF treatment leading to an hypertrophy of both SCG. This consistent with the hypothesis than NGF is the retrograde trophic agent for the sympathetic nervous system in the developing animal.
在大鼠6日龄时挤压颈上神经节（SCG）的节后神经干，导致肾上腺素能神经元轴突的分裂，这会引起SCG的永久性萎缩，表现为总蛋白含量以及酪氨酸羟化酶和多巴脱羧酶活性持续下降。在7至21日龄期间，以10微克/克/天的剂量给单侧轴突切断的大鼠施用神经生长因子（NGF），会导致正常和轴突切断的SCG均肥大。在治疗期结束前，两个SCG中的总蛋白含量和两种酶的活性都有逐渐升高。治疗停止后，总蛋白含量和两种酶的活性逐渐下降，4周后达到稳定水平。与未治疗的对照SCG相比，治疗过的未手术SCG达到的水平仍然升高。轴突切断并治疗的SCG的生化参数与未治疗的对照SCG大致相同，且比未治疗的轴突切断的SCG高得多。这些最终水平在治疗停止后至少持续56天。动物在6日龄轴突切断后出现持续性上睑下垂，但用NGF治疗可在11周龄时实现功能恢复。有人提出，在发育过程中，通常存在一种因子从靶细胞向神经元胞体的逆行转移，如果建立了适当的连接，该因子可使神经元存活。未能建立这样的接触会导致细胞死亡。正常发生的细胞死亡以及轴突切断导致的细胞死亡，都可以通过NGF治疗来预防，从而导致两个SCG均肥大。这与NGF是发育中动物交感神经系统的逆行营养因子这一假设一致。
