Hoyle G W, Mercer E H, Palmiter R D, Brinster R L
Laboratory of Reproductive Physiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.
Neuron. 1993 Jun;10(6):1019-34. doi: 10.1016/0896-6273(93)90051-r.
The effects of nerve growth factor (NGF) on sympathetic axon growth were investigated by generating transgenic mice in which the beta subunit of NGF was expressed in sympathetic neurons using the human dopamine beta-hydroxylase (DBH) promoter. In DBH-NGF mice, the sympathetic trunk and nerves growing to peripheral tissues were enlarged and contained an increased number of sympathetic fibers. Although sympathetic axons reached peripheral tissues, terminal sympathetic innervation within tissues was decreased in DBH-NGF mice. This effect could be reversed in the pancreas by overexpression of NGF in pancreatic islets. The observations are consistent with a model in which NGF gradients are not required to guide sympathetic axons to their targets, but are required for the establishment of the normal density and pattern of sympathetic innervation within target tissues.
通过构建转基因小鼠来研究神经生长因子（NGF）对交感神经轴突生长的影响，在这些小鼠中，利用人多巴胺β-羟化酶（DBH）启动子使NGF的β亚基在交感神经元中表达。在DBH-NGF小鼠中，交感干和向周围组织生长的神经增粗，且交感纤维数量增加。尽管交感神经轴突到达了周围组织，但DBH-NGF小鼠组织内的交感神经终末支配减少。在胰岛中过表达NGF可使胰腺中的这种效应逆转。这些观察结果与以下模型一致：即引导交感神经轴突到达其靶标的过程不需要NGF梯度，但靶组织内正常密度和模式的交感神经支配的建立需要NGF梯度。
